Where do you get your news? I'm a software developer.  Many of us get our news from http://news.ycombinator.com

Where do cogsci people get their news from?  I'd like to read the latest trends and discoveries in cogsci research.

I'm not sure how helpful my answer will be, but I get my "news" from scanning journals related to my interests.  I look through 1) broad review journals, 2) broad empirical journals and 3) more specific empirical journals.

In general, I find that popular media outlets do a poor job of reporting on research in psychology/neuroscience (but hopefully someone else has some idea of reliable/quality news outlets).

Broad review journals that I tend to look at include:

Trends in Cognitive Sciences
Current Directions in Psychological Science
Perspectives on Psychological Science
Emotion Review
Behavioral and Brain Sciences
Psychological Review
Psychological Bulletin
Psychological Inquiry
Personality and Social Psychology Review

Then there are the broad empirical journals:

Psychological Science   (studies from this journal appear very often in the news)
Clinical Psychological Science
Nature (usually hardcore neuroscience or behavioral economics)
Science (occasionally get a fun psych study here, which will be heavily advertised on the news)
Proceedings of the National Academy of Sciences (PNAS has a good psychological and cognitive sciences section)
Neuroimage
Journal of Personality and Social Psychology

And the more specific empirical journals (for me, mostly related to emotion):

Emotion
Cognition and Emotion
Social, Cognitive, and Affective Neuroscience

Looking at journals like these may not be too appealing if you want something quick and easy to read.  But I hope that this is useful to you in some way. :)


Why is deltaE not used as a measure of error? I've recently read a few articles pertaining to visual memory. Most of them (e.g. https://doi.org/10.1167/9.10.7) use the continuous color recall task where they ask participants to recall the color of an object by clicking on a color wheel. They use as measure of error the angular distance between the participant's response and the actual angle on the colorwheel of the object's color.

Why use this dependent variable? In the industry, people use deltaE to determine the color difference between a product and a prototype.

Wouldn't it make more sense to also use deltaE as dependent variable in psychology? From what I've read, deltaE tries to be accurate for human color perception.

Delta E is used extensively in vision research, however the study you sited only tested hue recall (all samples and test responses were designed to vary in hue and minimally in luminance and saturation).

This is one possible criticism of the studies. One of the major improvements in Delta E 2000 is a hue dependent rotation. We are more or less sensitive to certain hue regions. While this is one source of criticism, they are generally relying on large color differences to differentiate successful trials vs. unsuccessful trials and Delta E does not have any meaning for large color differences.

A more accurate reinterpretation might be to say that they aren't calculating color differences at all but rather the variation of the response distribution and the underlying probability density functions. The variation analysis is not dependent on individual color difference calculations.


Improved Typing as a result of slight movement I've found that my typing performance (speed, accuracy, flow) are noticeably improved if I am swaying slightly, mostly side to side, in a non-regular manner.  I would estimate that the overall movement side to side is less than an inch.

This occurs for all typing tasks, and surprisingly also affects my piano-playing performance.  It is not necessary to be listening to music (though it can help), and only sometimes does the movement correspond to the actual typing itself.  I also find that if mistakes are made, this movement is disrupted, and that consciously re-starting the movement helps restore the induced state.

What could account for this effect?

I would personally suspect that it's acts to induce a sort of 'flow' state, but I'd like to know if this has been studied or even noticed elsewhere...

I personaly also play piano and see myself into that flow easly,

Check out what I just found

From: http://en.wikipedia.org/wiki/Flow_(psychology)

  Flow is the mental state of operation in which a person performing an
  activity is fully immersed in a feeling of energized focus, full
  involvement, and enjoyment in the process of the activity. In essence,
  flow is characterized by complete absorption in what one does

  (...)

  Components of flow

  Nakamura and Csíkszentmihályi identify the following six factors as
  encompassing an experience of flow.

  intense and focused concentration on the present moment merging of action and awareness
  a loss of reflective self-consciousness
  a sense of personal control or agency over the situation or activity
  a distortion of temporal experience, one's subjective experience of time is altered
  experience of the activity as intrinsically rewarding, also referred to as autotelic experience

  (...)

Check this out:

  Roy Palmer suggests that "being in the zone" may also influence movement patterns as better integration of the conscious and subconscious reflex functions improves coordination.

  (...)

  Music

  Musicians, especially improvisational soloists may experience a
  similar state of mind while playing their instrument. Research has
  shown that performers in a flow state have a heightened quality of
  performance as opposed to when they are not in a flow state. In a
  study performed with professional classical pianists who played piano
  pieces several times to induce a flow state, a significant
  relationship was found between the flow state of the pianist and the
  pianist’s heart rate, blood pressure, and major facial muscles. As the
  pianist entered the flow state, heart rate and blood pressure
  decreased and the major facial muscles relaxed. This study further
  emphasized that flow is a state of effortless attention. In spite of
  the effortless attention and overall relaxation of the body, the
  performance of the pianist during the flow state improved.


What brain regions are activated when a dream is remembered? Some people remember dreams, others don't. The same person can wake up with dream recall one day and without on other days. I know that the association between REM sleep and dreaming was initially established by awakening test subjects during REM and asking them what they remember.

My question is about the dream recall phenomenon – imagine a person is woken up from a dream while his brain is being scanned. What is the difference in brain region activations shortly before awakening between the case where a dream is recalled and a dream is not recalled? In both cases polysomnographic readings would conclude that REM is experienced and probability of dreaming is high.

I'm asking this question in relation to this question about working memory of the memory recall patient HM. As I heard about his case, I could not help but think that his "living in the present" seems very similar to the experience of dreaming. While dreaming, one does not have a clear memory of the past events, or any desire to even access this memory. I'm trying to understand: can the difference in dream recall for the same test subject be localized to some inhibition of hippocampus or another brain structure, similar to what HM had surgically removed?

Dreams are prone to be "episodic", where a continuous dream of say 20 minutes may contain several very distinct scenes (2–5 minutes each) that have no relation to each other. I'm interested if such dream changes involve the same mechanism that HM experienced when he was distracted.

Your memory of a dream would be an autobiographical memory, which is a memory system that is based on a combination of episodic memories and semantic memories. Autobiographical memories are memories of events that have happened to you, and thus are often retrieved from a first-person perspective. These are not the same thing as episodic memories, however, as episodic memories are contained in a separate memory system.

Your autobiographical memory knowledge base is distributed through neural networks in the frontal, temporal, and occipital lobes. The frontal lobes and anterior temporal lobes represent the more abstract or conceptual parts of the memory, and the occipital lobes/posterior temporal lobes represent the more sensory and perceptual details of specific events. These are predominantly represented in the right cortex. [1] Initially, a memory is formed in the left prefrontal region. Over time, this memory is 'moved' and held at a higher level in the posterior region.

However, there are more widespread activation patterns throughout the brain, and almost every region of the brain has been represented in at least one instance of autobiographic memory retrieval. [2] This lends itself to the belief that certain regions are used for certain types of retrieval, such as re-living experiences associated with the memory versus retrieving factual information from the memory.

Dreams themselves are not episodic memories. During REM sleep, there are specific brain regions that appear to be affected; in particular, there is increased activity in the formation of the hippocampus and decreased activity in prefrontal regions. There appears to be no temporal lobe activity, which implies that 'dream memories' are not true episodic memories, but instead representative of episodic fragments (at best). One study [3] even found that the majority of dreams (>80%) were comprised of primarily autobiographical memories. This suggests that dreams themselves are comprised of fragmented and selective personal experiences, perhaps to aid in the assimilation of memories into the autobiographical memory schema.

Sources used:

[1] Conway, M.A., Pleydell-Pearce, C.W., & Whitecross, S.E. (2001). The neuroanatomy of autobiographical memory: a slow cortical potential study of autobiographical memory retrieval, Journal of Memory and Language. 45, 493-524.

[2] Svoboda, E.; McKinnon, M.C.; Levine, B. (2006). "The functional neuroanatomy of autobiographical memory: a meta-analysis". Neuropsychologia 44 (12): 2189–2208.

[3] Malinowski, J. E. and Horton, C. L. (2014), Memory sources of dreams: the incorporation of autobiographical rather than episodic experiences. Journal of Sleep Research, 23: 441–447.


Difference Between Schema and Mental Model What are the differences between a schema and a mental model? Do they overlap, or is the mental model a subtype of the schema?

At a high level, schemas and mental models are of a kind in cognitive science. You can think of both as cognitive or representational structures that aid in the storage and retrieval of information. Schemas were introduces earlier (Bartlett, 1932), and were followed by concepts such as scripts and frames (Schank & Abelson, 1975; Rumelhart, 1972). All of these, in general, describe the way that information can be structured in the mind such that we can easily navigate complex yet familiar situations, as well as adapt to and learn how to navigate novel situations.

I usually attribute the introduction of mental models to Johnson-Laird (1980, 1983). A lot of this work was based on evidence of spatial representational structures in peoples' minds when they do things like read a story, and (since I'm a language guy), these ideas were further extended to situation models of text, which suggest we hold mental representations outside of the realm of space and time, and into causality and goals (e.g., Kintsch & van Dijk, 1983; Zwaan & Radvansky, 1998; and others such as Glenberg, Morrow, ...). I kind of think of this work as extending more abstract notions such as schemas into people's actual memories and experiences.


How was fMRI performed before EPI became available? How did fMRI work before Echo-planar imaging (EPI) became available? EPI allows fast imaging and high temporal resolution, but it became commercial in the second half of the '90s. How was it possible to perform fMRI in the early '90s and to observe neural activation using slow gradient echo imaging which requires 3 minutes to acquire a whole image?

Short answer
Older image collection techniques like GRASS and FLASH are slower than EPI, but still fast enough to operate within the time span of the neurovascular delay.

Background
The speed of fMRI processing is an important limitation to what processes can be investigated with this technique. Figure 1 shows a number of physiological processes along with a time line of a number of key fMRI strategy developments  (source: Cohen). Figure 1 shows a steady decrease in MR imaging times in the first decade of its conception. The cerebral blood flow response used in fMRI BOLD imaging typically begins within ~500 ms and peaks 3–5 s after stimulus presentation (Hilman 2014). fMRI BOLD is based on the neurovascular coupling, referring to the relationship between local neural activity and subsequent changes in cerebral blood flow (CBF). Any imaging technique that utilizes the neurovascular coupling, notably fMRI BOLD, should be fast enough to operate withing= the time window of the neurovascular delay.

Echo-planar imaging (EPI), was already known by 1977, but was implemented not until 1990 for fMRI. EPI collects image data in 40 to 150 milliseconds and hence is more than sufficient to obtain a BOLD response. Earlier image collection techniques (gradient echo methods) such as Fast Low Angle Shot (FLASH) and Gradient Recalled Acquisition in Steady State (GRASS) are much slower and need several hundreds of ms (FLASH) or several seconds (GRAS) to obtain an image. Nonetheless, these processing times are still sufficient to obtain a cerebral blood flow response.

Fig. 1. Duration of various physiological processes (top) and development of imaging techniques and their image collection times (bottom). The neurovascular peak delay (around 8 sec as depicted here) has a time window sufficiently long to be recorded by GRAS, TurboFLASH and EPI have processing times within that time window and can theoretically be used for fMRI. source: Cohen

Reference
- Hilman, Annu Rev Neurosci (2014); 37: 161–81


How to learn about children using hitting affectionately When I am about to leave, my youngest son will show affection by hugging me before I leave. When we are playing a game and he is really enjoying it, he will actually smile at me and hit me really quickly maybe 5 times a row. Sometimes this coincides snuggling his head into my body.

Initially I thought he was being angry or acting out, it has become clear that he only does it a happy face while we are doing something fun. (And not in an "I am overwhelmed" kind of way. Lately I respond by returning a hug instead of giving him a surprised or irritated face, and he likes that).

Anyway, when I try to google to understand this, keywords such as "affectionate hitting" simply return thousands of "anti-parent hitting children sites". Is there an term for when children do this so I can find more helpful thoughts/discussion about this?

The search term "children hitting for fun" seems to yield the results you may want although the results seem to come from sites such as mumsnet.

An aspect to this phenomenon is that this behaviour may lead to bullying behaviour later on in life if the right responses are not given when this occurs.  The child needs to learn the cause and effect of hitting.

Typing the same term in Google Scholar gives research articles on dealing with bullying.


Diet for brain stimuli I want to ask which foods or supplements enhance brain function and how,like for example protein is good after a muscle workout what is the equivalent for the evolving of the brain,antioxidants are said to be good, but why.

Also,do you have in mind any constructive book or article from which I can elaborate myself.Furthermore do exist diet for brain stimulation?Thanks in advance.

Assuming a diet is not deficient; this is a brief overview of some of the dietary needs for optimal brain function.

Maintaining glucose levels is necessary to maintain healthy brain function.
There is substantial research on the positive effects of omega 3
fatty acids on brain function.
Vitamin and mineral  deficiencies can cause disruption to brain function (note so can excesses).

Glucose:

This article gives some good detail about how to maintain healthy glucose levels; with discussion of glycaemic index and maintaining a steady release of glucose from the breakdown of complex carbohydrates.

Nourish - Carbohydrates Fuel Your Brain

  Glucose, Learning and Memory - Study

  Psychology professor Paul E. Gold has researched the stability of glucose levels in the brain. Working with Ewan C. McNay , they found that as rats went through a maze, concentrations of glucose declined in the animals' hippocampus , a key brain area involved in learning and memory – even more dramatically so in older brains.

  Except under conditions of starvation, it was thought that the brain always had an ample supply of glucose. "While this is the case in terms of consciousness, the new findings suggest that glucose is not always present in ample amounts to optimally support learning and memory functions," said Gold, who is director of the Medical Scholars Program in the University of Illinois College of Medicine.

  "The brain runs on glucose. Young rats can do a pretty good job of supplying all the glucose that a particular area of the brain needs until the task becomes difficult," explained McNay, a postdoctoral researcher in psychology at Yale University. "For an old rat given the same task, the brain glucose supply vanishes out the window. This correlates with a big deficit in performance. A lack of fuel affects the ability to think and remember."

Brain Energy Metabolism
An Integrated Cellular Perspective
Pierre J. Magistretti, Luc Pellerin, and Jean-Luc Martin

  Glucose is the obligatory energy substrate for brain and it is almost entirely oxidized to CO2 and H2O.

Role of glucose in regulating the brain and cognition.
P E Gold

  Extensive evidence indicates that relatively modest increases in circulating glucose concentrations enhance learning and memory processes in rodents and humans.\

Omega 3 fatty acids:

  Lipids (fats)- some fats are essential for proper brain function. Two lipids especially critical to the brain are the n-6 and n-3 fatty acids. Low levels of n-3 cause visual problems by badly affecting the retina. Studies in rats have shown that diets without n-3 fatty acids cause learning and motor disabilities and may damage systems that use the neurotransmitters dopamine and serotonin in the frontal cortex. The n-6 fatty acids affect neurotransmitter release and contribute to the ability of neurons to use glucose for energy.

Brain foods: the effects of nutrients on brain function
Fernando Gómez-Pinilla  doi:  10.1038/nrn2421

  ... a diet that is rich in omega-3 fatty acids is garnering appreciation for supporting cognitive processes in humans and upregulating genes that are important for maintaining synaptic function and plasticity in rodents. In turn, diets that are high in saturated fat are becoming notorious for reducing molecular substrates that support cognitive processing and increasing the risk of neurological dysfunction in both humans and animals.

Vitamins:

From:
B vitamins and the aging brain.
Selhub J, Troen A, Rosenberg IH.  doi: 10.1111/j.1753-4887.2010.00346.x.

  Deficiencies of the vitamins folate, B(12) , and B(6) are associated with neurological and psychological dysfunction and with congenital defects. In the elderly, cognitive impairment and incident dementia may be related to the high prevalence of inadequate B vitamin status and to elevations of plasma homocysteine

The Vitamin You Need for a Sharp Brain as You Age
Dr. Mercola

  Accordingto the latest research, people with high levels of markers for vitamin B12 deficiency were more likely to score lower on cognitive tests, as well as have a smaller total brain volume, which suggests a lack of the vitamin may lead to brain shrinkage

Vitamin B12, cognition, and brain MRI measures: a cross-sectional examination.
Tangney CC, et al  doi: 10.1212/WNL.0b013e3182315a33.

  Concentrations of all vitamin B12-related markers, but not serum vitamin B12 itself, were associated with global cognitive function and with total brain volume.

Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease.
Eyles DW, Burne TH, McGrath JJ.  doi: 10.1016/j.yfrne.2012.07.001

  Increasingly vitamin D deficiency is being associated with a number of psychiatric conditions. In particular for disorders with a developmental basis, such as autistic spectrum disorder and schizophrenia the neurobiological plausibility of this association is strengthened by the preclinical data indicating vitamin D deficiency in early life affects neuronal differentiation, axonal connectivity, dopamine ontogeny and brain structure and function. More recently epidemiological associations have been made between low vitamin D and psychiatric disorders not typically associated with abnormalities in brain development such as depression and Alzheimer's disease

The following link gives a good overview of vitamin deficiencies and toxicities.

Fat-Soluble Vitamins: A, D, E, and K
by L. Bellows and R. Moore

  Fat-soluble vitamins: A, D, E, and K — are stored in the body for long periods of time, and pose a greater risk for toxicity than water-soluble vitamins. Fat-soluble vitamins are only needed in small amounts.

Note: that, within all scientific research,there can be research that is "conclusive", but   it is also important to be mindful, that not all findings are conclusive.

Vitamin D and cognitive performance in adults: a systematic review.
Annweiler C, et al   doi: 10.1111/j.1468-1331.2009.02755.x.

  . Three studies showed four significant positive associations between serum 25OHD concentrations and global cognitive functions, whereas three other studies exploring specific aspects of cognition showed 11 non-significant associations. This systematic review shows that the association between serum 25OHD concentrations and cognitive performance is not yet clearly established. The inconclusive results of the reviewed studies could be due to methodology, types of the cognitive tasks used and/or the cellular mechanisms of vitamin D.


How to estimate an expected effect size for a planned psychology study? When planning a psychological study, researchers are often asked to formulate an estimate of  expected effect sizes for important hypotheses in the study. This might be the expected group mean difference (e.g., Cohen's d), the correlation between two variables, the odds ratio, or any number of other effects of interest.
Such estimates can then link into power analysis and sample size calculations.

However, often formulating such an estimate is a difficult task. The exact study has not been performed before. Meta-analyses may only be partially related to the hypothesis of interest. Various modifications to the design might be theorised to change the effect size from previous studies. This leads to the question of how to systematically integrate such information to formulate an expected effect.

What is a good strategy for formulating an expected effect size in a psychological study, particularly where the study has not been performed before?
Are there any scientific articles that attempt to elucidate best practice in effect size estimation in a psychological research context?

Note: A student recently asked me this question, thus I thought I'd post it here to draw on the expertise of others. I will post my answer below as well, but hopefully other people add answers also.

The purpose of reviewing the literature for effect sizes is to form an estimate of what effect size you might expect in your present study.

Existing meta-analysis: The principles and techniques of meta-analysis provide a good starting point for generating a predicted effect size.
If a meta-analysis has already been conducted, then the estimated population mean and confidence intervals of effect sizes is a useful piece of information.
In some cases there will also be a moderator analysis reported which tests whether the effect size varies as a function of the moderator (e.g., adults versus children; lab versus field, etc.). If your study matches one level of an influential moderator, then it may be worth weighting estimates more by the estimated effect size for that moderator.

No existing meta-analysis: If no meta-analysis exists or if one exists but is out of date, then you may want to perform your own meta-analysis. There are several great books on meta-analysis. I've personally found Borenstein et al (2011) to be a good introduction and Hunter and Schmidt (2004) to be useful  particularly if you are interested in correlations and various corrections. Here is a link to an overview of meta-analysis.
Conducting a rigorous meta-analysis for publication is a technical and resource intensive process. However, if all you want is a ball-park estimate of expected effect size for sample size and study design considerations (i.e., your not doing an explicit meta-analysis publication), then it may be more pragmatic to just do a quick informal meta-analysis.  In some cases there might only be one or a few studies which are similar to your study. In this case, the meta-analysis can be very simple.

Generalisation: Another issue that comes up is generalisation. Students sometimes say to me that there have been no other studies like the one being conducted. This may be true, but at some level of generality this is almost always false. If a study is about a particular training program in the work place, then a meta-analysis of training in general may be informative. If the intervention has only been used with teenagers and is now being applied to adults, the meta-analysis of teenagers would be relevant. Broadly, theory should be applied to assess the likely generality of any broader research to the present study.

Theory: Theory is important in many respects. Theory may suggest that a particular modification to the design should increase or decrease the effect size relative to a previous studies.

Aggregating estimates: In general it is is important to consider how different effect size estimates should be aggregated. The more similar a previous study is to the present study, the more weight should be given to any effect size estimate. In this case, similarity requires theoretical judgement about what are the important factors that might moderate the effect. Similarly any aggregation needs to be mindful of sample size considerations where larger sample sizes will increase the precision of the estimate in any given study. Thus, at the ultra-specific, the present study may be an exact replication of a previous study. At another level, there may be meta-analytic evidence from similar studies. At an even broader level Jacob Cohen reluctantly proposed various rough rules of thumb of what to expect for small, medium, and large effects in behavioural science studies.

Importance of uncertainty: Another point is that you don't actually know the population effect size for your study. That's why you are doing the study. There will always be uncertainty about your effect size estimate. It can even be useful to quantify that uncertainty either using meta-analytic confidence intervals or something more ad hoc.
This is analogous to the concept of a subjective bayesian prior probability on a parameter of interest. See for example, this discussion of eliciting priors from experts. Meta-analysis provides some methods for quantifying uncertainty in an effect size estimate, but this may not be entirely appropriate given that you are not trying to generalise to the variation in the whole world of effect sizes. Rather you are trying to generalise a prediction for a specific study, and you may be pooling many different pieces of information, some quantitative, and some qualitative.

By way of example, I do research on personality faking. I am aware of a meta-analysis of the mean effect size of faking versus honest personality responses (e.g., perhaps around d = .6). However, I also know from previous research that the type of faking instructions makes a big difference to the expected effect size (e.g., if you tell people to fake you often get approximate d = 1.0 and if you just put people in a context with a motivation to fake you get approximate d = .3). Thus, If I were calculating expected effect size for any given study I would combine knowledge of the nature of my faking instructions with various meta-analytic estimates. I'd weight my own previous studies highly because they typically share more similar features (e.g., same personality test, similar participants, etc.) than the general literature. I'd also acknowledge the uncertainty in my estimate.

References

Borenstein, M., Hedges, L. V., Higgins, J. P., & Rothstein, H. R. (2011). Introduction to meta-analysis. Wiley.
Hunter, J. E., & Schmidt, F. L. (2004). Methods of meta-analysis: Correcting error and bias in research findings. SAGE Publications, Incorporated.


When faced with a choice and trying to make a quick decision, are 2 options better than 3 or more options? Bastardi & Shafir (1998) show how too much data disabilitates your decision making. There is also the popular Paradox Of Choice argument.

However, I can't find a reference stating that, when faced with a decision, 2 options are better than 3 or many options. It makes sense--you either like one of the options less or more than the other, and can then come to a quicker conclusion.

Is my intuition correct? If so, Could someone please point me in the direction of a thesis or paper which shows that?

UPDATE

I just found this paper and will update my question (or answer it!) if I find an answer.

UPDATE 2

I realise that the converse can be true as well, especially in the scenario when obtaining something, like the latest tablet. For example, bias and culture could make it really easy for you to discount the vast majority of options (e.g. anything not made by Apple), but then you struggle to make the final decision (e.g. shall I get an iPad 64GB or an iPad 4G?).

As Piotr mentions in the comments, you must operationalize "better".

Total time spent making a decision is likely to increase as the number of decision alternatives increase. This is known as Hick's Law.

If each choice has some objective value, then the maximum possible value that could be attained is likely to increase as the number of decision alternatives increase. This is probability.

The truth is not so clear cut. Each choice has some subjective value that is governed not only by its own intrinsic properties, but by comparison to other choices. Barry Shwartz, author of The Paradox of Choice, will tell you that having other choices available to you can increase the experienced regret post-decision, which lowers the subjective value of the choices.

There's also a speed-accuracy trade-off. If a decision needs to be quick, as you say, there is some cost associated with time that needs to be subtracted from the value of the chosen option.

Overall, it would be too simplistic to say "2 choices are always better than one", or vice versa. The answer, as usual, is "it depends".


Is short-term memory theoretically possible to with spiking neurons? So I close my eyes, turn around, open them for just a blink and close again. I have observed a chair. I can't tell you how the chair looks like in detail, but I can more or less tell its shape and color. What's more, if I'm not disturbed, I can remember that shape and color for at least a minute.
What if I wanted to construct a device that could repeat this process. With digital hardware its not too hard - take a digital camera and a solid state memory device. For every bit of info in my solid state drive, I can call the operation "store" and my bit will be stored, or "erase" and it will be erased. Don't know how reliably each physical bit works with current technology, but given sufficient number of physical bits per logical bit I can theoretically make a device that will store my picture for as long as I want.
What about building a spiking neuronal network to do the same thing? I have tried some naive approaches, and I arrive at a fundamental problem: spiking neuronal networks seem to have almost no inertia on the fast timescale. A neuron only fires while there is sufficient input. When input is gone, it no longer fires (besides some resting state activity). I can construct a network with recurrently-connected neurons, in which case, in principle, the activity of the network could sustain itself after the input is gone. However, depending on the parameters of the network I observe a rapid switch between two very extreme behaviours. In one case, the feedback strength of the network is too weak, and the activity drops as soon as the input is gone. In the other, the feedback weight is too strong, and the activity of the network quickly reaches some maximal firing state independently of which exact input the network has received. These transitions happen exponentially fast. Theoretically, there are adaptive control mechanisms in neuronal networks, such as inhibition and synaptic plasticity. However, I am struggling to understand how such mechanisms can ever be fast enough to compensate for the sudden increase or drop of input.
TL;DR: Naively neuronal networks do not seem stable enough to implement robust short-term memory. What are the known mechanisms that nevertheless make it possible?
Note: I'm not asking how exactly short-term memory works. I am aware that nobody really knows. I'm asking for intuition to help disprove my argument that it should not work when implemented using neurons.

While we don't entirely know how all aspects of working memory operate, experiments show that a subset of cells in the brain exhibit persistent activity during working memory tasks.
Here's an example from a review by Curtis & D'Esposito:

This is a task in panel (a) where there is a cue presented briefly (marked by "C"), and then the monkey needs to remember the cue (during the time marked by "D"), and finally at time R the targets appear and the monkey can make a response.
We see in spiking recordings from monkeys that there are cells in dorsolateral prefrontal cortex that are activated not only by the cue and during the response, but they have persistent activity during the delay period. In human studies we can't ordinarily place electrodes but part (b) shows a similar study using fMRI, and the colored areas on the brain indicate brain areas that demonstrated more blood flow (marking metabolism) during the delay period, which includes areas of the same brain region as the monkey experiments.
The explanations are recurrent network activity and bistability: a population of cells that is excited can continue to excite each other and remain active until stopped (see for example attractor networks for a conceptual idea), as well as bistability in individual neurons where a neuron that reaches threshold continues to fire tonically rather than firing a single action potential, until firing is ceased via inhibition. Camperi and Wang 1998 is an excellent, clear review of these concepts with a straightforward mathematical approach to how you can model this in silico. It's probably more efficient to start from here rather than reinventing it on your own.
I also recommend other papers by XJ Wang who has done extensive work in this area. I also recommend you look at phase-space diagrams which can help conceptualize dynamic systems with stable properties (and which network parameters are necessary for stability), they come up a lot in theoretical neuroscience. Dayan and Abbott's Theoretical Neuroscience is also a good starting point if you can find a copy.

Camperi, M., & Wang, X. J. (1998). A model of visuospatial working memory in prefrontal cortex: recurrent network and cellular bistability. Journal of computational neuroscience, 5(4), 383-405.
Curtis, C. E., & D'Esposito, M. (2003). Persistent activity in the prefrontal cortex during working memory. Trends in cognitive sciences, 7(9), 415-423.


Can we enter data at the speed of thought? I have the subjective personal experience that the speed at which I can enter information in a computer through a keyboard is so slow and my thoughts "run" so fast, that I find it an especially frustrating experience to compose a text on a computer or do a translation.

Is there any research studying the effects of computer keyboard data entry speed compared to the speed at which thinking happens (or the speed of speech, the latter measurable) or just some paper elaborating on a correlation between the speed of data input and the subjective feeling of smooth mind work?

Maybe research with stenographers (supposed to be able to write at the speed of speech) would be a good direction? An article suggesting such correlation:  (Plover, the Open Source Steno Program: Writing and Coding With Steno).

I am unfamiliar with such research. However, considering this from a User Interface design perspective, as well as from a cognitive perspective, I would add one bit of clarification to the question.

Can we enter data at the speed of organized thought?

If the limitations in user interface technology are overcome to the point where the input gate is no longer the limitation, it is quite possible that we would discover that our thought processes are so chaotic as to render the new technology virtually useless.

As support for this I would point out that sitting and typing a message, while slow, is already a method by which thoughts evolve into lucid communication.


Neurosurgically grown neural link between two brains? I guess it's possible to surgically restore neural connection after a trauma (e.g. a severed hand can be reattached if done quickly).

And, from history of evolution of hominids, it seems that just by increasing brain size by 30% it's possible to develop a radically higher level of cognitive abilities.

Putting these two ideas together, I wonder if anyone tried to grow a neural link between two separate brains. Maybe even a narrow, low-bandwidth wisp of neurons between two brains would adapt itself to expand the consciousness. I wonder what will be the effect of such a 100% increase in brain size. And if it works, we can connect three brains, then four, five, etc. Of course, these "compound people" would have trouble moving around as they won't be able to separate their heads more than few centimeters...but if the tradeoff is that they become exponentially more sentient...?

Could you please point to some research performed in this direction?
Is it even legal in developed countries? Thank you.

Research exists on craniopagus twins, maybe most notably Tatiana and Krista, who seem to share sensory input somewhat. I doubt that connective mechanisms such as this abnormal case would suffice to permit "compound cognition" in ways that would enhance cognitive ability similarly to your point about hominid evolution. Your relatively simple proposal for a connective cord of neurons strikes me as roughly equivalent, though more complex connections may not be entirely unfeasible in the long run.

Before I move on to speculating about that, consider a few other points from cognitive neuroscience thus far. Plenty of split-brain research (on people and animals with dysfunctional corpus callosums) exists as well, little of which shows what I would call "radical effects on cognitive abilities". Results are somewhat more subtle than that: e.g., involving object recognition more than what laypeople would recognize as intelligence, especially social communication and basic reasoning, which remain relatively intact. You might also be surprised at the modest effects of losing an entire cerebral hemisphere: again, it's not what I would call a 50% reduction in cognitive ability, at least as we understand and use such abilities in modern social contexts.

Non-biological methods are already being experimented with for brain-to-computer and even human brain-to-brain interfacing (Armstrong & Ma, 2013), but we're some distance away from really augmenting cognitive abilities through such methods in the way evolution seems to have augmented them in hominids. Consider also that evolution seems to have proceeded in far more complex manners than those by which we're connecting brains now. Changes occurring organically throughout the brain over millions of years of natural selection may have developed our cognitive abilities well beyond those of smaller-brained animals, but these changes have probably been much more sophisticated than simply wiring disparate parts together, let alone only one part to only one other. Cognitive processes are functionally dispersed broadly across our incredibly complex neural structures; we definitely use more than 10% of our brains. There's really no particularly promising hub-of-all-cognitive-ability through which one could connect and expect to provide consciousness-wide augmentation (that I know of), nor would it be as simple as connecting one brain to another.

To throw in a halfhearted computer metaphor, consider how little processing ability is gained simply by connecting two computers by LAN cable. In very many ways, computer processing augmentation has had to proceed much more incrementally, component by component. Multi-core processors and several sticks of RAM per computer are commonplace now, but to truly augment computing performance with these, fundamental architectural changes in connective design have necessarily occurred. Far more than one wire connects these compound components.

Thinking in this manner might pave the way to future innovations that may someday achieve the effects you have in mind. Transhuman cognitive augmentation research is rapidly advancing in very many directions, some of which may bear satisfying similarities to your idea. They're all well beyond the scope of my knowledge or of this answer though, so I'll just toss some Wikipedia links at you to get things started. Please feel welcome to ask separate questions to follow up on cyberpsychological topics; I find them all very exciting, and would be very eager to explore them further with you and our community!

Intelligence amplification
Cyborgs, cybernetics, and cyberware

Exocortex – artificial external augmentation system for high-level cognitive processes
Neuroprosthetics – devices to substitute motor, sensory, or cognitive modalities

Visual prosthetics

Artificial brains

The Blue Brain Project – a molecular reverse-engineering of the mammalian brain
Artificial intelligence – arguably more on-topic at the dedicated AI Stack Exchange

Hierarchical temporal memory – online machine learning structural neocortical model

Wetware computers – built from organic, living neurons!

Nootropics – cognition, memory, intelligence, motivation, attention, and concentration drugs

See a related question, Do smart drugs (nootropics) make you smarter?
Ampakines – compounds that enhance attention span, alertness, learning, and memory

Transcranial direct-current stimulation

See a related question, Can learning be facilitated by transcranial magnetic stimulation?

Mind uploading – copying mental content from a brain substrate to another computational device

Depends on brain reading / fingerprinting / thought identification

Augmented reality

Consumer brain-computer interface devices
Neurofeedback – illustration of brain activity to teach self-regulation
Augmented learning – adaptive learning environments
Electronic learning
Web-based simulation
Wearable computers

Head-up displays – transparent data displays that accommodate users' usual viewpoints

Bionic contact lenses and virtual retinal displays
Optical head-mounted displays
EyeTap
Google Glass

Reference

Armstrong, D., & Ma, M. (2013, August 27). Researcher controls colleague’s motions in 1st human brain-to-brain interface. Washington University: News and Information. Retrieved from http://www.washington.edu/news/2013/08/27/researcher-controls-colleagues-motions-in-1st-human-brain-to-brain-interface/.


Do other forms of bias have their own terminologies, similar to "Stockholm Syndrome"? Three examples would be:

Someone who makes an expensive purchase, and even when they are met with objective facts stating why it was a inferior purchase, they continue to sing it's praise.

Someone who blindly follows and defends their political party affiliation, even when confronted with facts showing why it's a bad affiliation.

Someone who commits to a lifestyle choice, and even when confronted with facts showing why it's a bad choice, they refused to believe it.

I know an all encompassing term might be cognitive bias, but I was hoping for specific terminologies to the three types of biases above.

Yes, Wikipedia even has a list.

Someone who makes an expensive purchase, and even when they are met with objective facts stating why it was a inferior purchase, they continue to sing it's praise.

This is related to the endowment effect and sunk costs fallacy.

Someone who blindly follows and defends their political party affiliation, even when confronted with facts showing why it's a bad affiliation.
Someone who commits to a lifestyle choice, and even when confronted with facts showing why it's a bad choice, they refused to believe it.

These are both fairly closely related, and there are several types of bias that could contribute to either - you'd have to have more information about what led to that bias, as you are sort of describing the 'symptoms' rather than causes. Conservativism bias, confirmation bias, bandwagon effects, social comparison biases, selective perception, reactance, and more.
However, I would also encourage you to be wary of the many forms of bias that cloud your judgment of others, as well. If you are perceiving people as being part of a 'bad affiliation' or making a 'bad choice' you should consider that your own biases may cause you to discount the reasons for those decisions. You may value different things than they do, and those differences in values may or may not be related to cognitive bias per se, but also simply individual differences in personality, life experience, etc.


Are there theories on how vocabularies for the Semantic Pointer Architecture are created? The semantic pointer architecture is a vector symbolic architecture where high-dimensional sparse vectors represent concepts. These concepts can be mathematical, linguistic or sensory. In all of the experiments I've seen these vectors are assigned randomly

In the case of mathematical and linguistic, are there any theories or experiments investigating how these vectors may be formed? Is this a relevant topic for investigation? If not, why?

I do not know for sure, but I believe that the vectors would be created in a domain-specific manner.  Vectors in the visual system would be created in a way that is particular to the needs of visual processing, etc.  The reason why the vectors are represented as random in the semantic pointer architecture, is because from the point of view of the architecture itself, the information encoded in the vector is irrelevant.  What is relevant is how to manipulate those concepts once they are already formed.


Compared efficiency of different spaced-repetition memorisation techniques Spaced repetition is a memorization technique that works by reviewing question/answer pairs according to a schedule that depends on performance.

Be it software or paper flashcards, there are various techniques to calculate the review schedule. For instance: Leitner, SM0, SM2, ... new techniques appear from time to time.
Each new scheduling technique is trying to surpass the others, the goal being to calculate the intervals smartly, for instance so that a question is shown just before the student forgets the fact.

Is there work comparing the "efficiency" of some of those scheduling techniques? (few reviews, well-memorized) Preferably research involving a reasonable number of human experiments.

A quick Pubmed search shows a couple of potential useful papers. The more promising:

Karpicke, JD., & Bauernschmidt, A. (2011) Spaced retrieval: absolute spacing enhances learning regardless of relative spacing J Exp Psychol Learn Mem Cogn. 37(5):1250-7
Toppino, TC., Kasserman, JE., & Mracek WA. (1991) The effect of spacing repetitions on the recognition memory of young children and adults J Exp Child Psychol. 51(1):123-38.


What are the most effective psychological techniques for unlearning information What are the most effective psychological techniques for unlearning information?

Let me given you a simple example for clarity's sake:
In high school, you learn that electrons orbit around a nucleus, whereas in reality electrons are actually at every point of the orbit at the same time. How would you go about unlearning the initial fact learnt in high school? It seems that the earlier fact is retrieved subconsciously since it has become a habit.

In the case of this simple example, it seems to be easier to replace the earlier fact. However, this appears to be problematic when dealing with more advanced concepts such as unlearning a simplified version of how fMRI functions.

From the book memory the following extract might be helpful:

  …, the association between a stimulus and a trace will be weakened
  whenever that trace is retrieved inappropriately. In effect, the bond
  between the cue and the target gets “punished”. For example, suppose
  that you try to retrieve the new password to your e-mail account.
  According to the unlearning view, if you recall your old password and
  realize the mistake, the association between the cue password and the
  original password will get weakened, decreasing the chances that it
  will pop up again in the future. If the old password is punished often
  enough, the association might grow so weak that it will no longer
  activate that trace; stimulus will be decoupled from the response.

So if the old information is punished many times it will start to loose its strength, and if at the same time the new information is rewarded, the new information will replace the old.

Reference:

Melton, A., & Irwin, J. (1940). The influence of degree of interpolated learning on retroactive inhibition and the overt transfer of specific responses. American Journal of Psychology , 53, 173-203.


Why does campfire lighting look creepy? Various photography lighting guides state that when light is positioned above a face it looks natural, but when positioned below a person it looks unnatural or even "creepy".

This is sometimes used deliberately in movies to evoke fear.

The universal principles of design say that this is because we evolved on planet earth with a single sun, which is always above us.

But there are plenty of natural situations where light could come from under us. Such as being reflected off the ground, snow, or water, or just sitting around a warm campfire.

I'm just curious if there are any known psychological reasons why lighting under a face might look unnatural or "creepy"? Or could it be that it's such a staple of horror movies that we're primed to perceive it that way?

There are situations as you mentioned where light can be from below, but they are extremely rare in our evolutionary past. Fire is quite recent: remove that one. Reflections from water or snow would require very strong light from above, so those are essentially removed as well. I think the creepiness comes from the unfamiliarity. Also see the Uncanny Valley, which describes similar feelings in response to near-human representations https://en.wikipedia.org/wiki/Uncanny_valley

A good test would be with non-human animals. Do they find bottom-lit faces fear-inducing?


Is the theory of Information Metabolism a reasonable scientific theory? Background

I have been checking out various personality typing assessments lately when I came across a Personality typing system known as Socionics which aims at explaining relationships between people of different types. It's based on some of Freud's ideas, Carl Jung's Psychological Types and Anthony Kepinski's theory of Information Metabolism.

Socionics uses a mixture of all the above to create its own sound theory about human psyche for each type of person. Socionics is considerably different from MBTI and other typing systems in its approach largely due to ideas from Information Metabolism.

While digging out more about Information Metabolism theory, I have found out that it implies things like information that is exchanged between people are like inputs and outputs from our brain. Socionics theory seems to extend this concept saying "Psychological features such as attention, interests, memory and motivation are components of this theory of information metabolism", because people differ in the way they process information.

Whether our brain really has parts corresponding to information elements like that is a different question, but I first doubt the scientific reason behind the theory of Information Metabolism. It seems to be based on Freud's ideas (which seem like mere observations), but yet on the other hand speaks about parts of brain.

Questions

Is this theory of Information Metabolism based on Scientific grounds?
Are there any theories/research like Information Metabolism that has been developed or in development and is/are scientific? Does CREATES brainset model qualify to be one such in development?
This may seem like a tangential question, but I will ask it because it's somewhat related: Do these Information Elements, provided they really exist, influence our facial expressions and body language while we interact with others?

The last question is to check out the validity of infamous Visual Identification used in Socionics communities for typing people by looking at them.

Other links

Wikipedia entry about Information Metabolism. (The resources in western community about Socionics and related theories are limited because the theory is largely developed in USSR and it looks like a counterpart of MBTI over there!)
A wiki about Socionics which has articles about the theory.
An excerpt from Carl Jung's Psychological Types which has been largely used in Socionics.

Is the theory of Information Metabolism a reasonable scientific theory?

Short answer: No.

A literature search of Google Scholar and Web of Science for "information metabolism" finds no empirical evidence to support the theory. Furthermore, it appears that the theory of information metabolism is virtually only embraced directly by the author, Kępiński, himself.

However: It is based on scientifically sound principles of dissipative systems, thermodynamics and negentropy, as proposed by Nobel prize-winning physicist Ilya Prigogene. In some sense, though, it is based on science in the same sense a movie may be based on a true story. It's not a trivially wrong theory, but there does not appear to be any concrete support.

CREATES and theories resembling information metabolism theory

CREATES does not appear to have any scientific basis or relation to information metabolism theory whatsoever. However, the link you provided cites Carnot’s principle as a basis for the theory of information metabolism:

  “the organism is an open system and its negentropy rises or falls as results of processes described by the laws of life conservation and species conservation, respectively”

This is very similar to the principles of more modern embodied dynamical systems approaches to explaining behavior, such as the ecological psychology of Mace, Turvey and Shaw. Both ecological and information metabolic approaches appear to be epistemologically dynamicist, and therefore share an epistemological stance. They appear to differ strongly on the content theory of the cause of behavior (i.e., on what constitutes a meaningful scale for behavioral analysis): information metabolism theory draws more heavily on Freud and Jung, while ecological psychology draws on the work of James J. Gibson.

Concluding remarks

Information metabolism theory is not a reasonable scientific theory in 2015, but neither was it scientifically stillborn in 1970. It appears to have been a theory invented before its time; in this, it is also like Gibson, who similarly lacked both the theoretical and mathematical tools to specify and formalize ideas. The popularization of those tools in behavioral science would eventually lead to the development of ecological psychology as a full fledged school of thought in the decades after Gibson's death.

In the case of information metabolism theory, however, it appears that either the theory was entirely subsumed into socionics and therefore no longer exists as an independent theory, or simply that no one took up the mantle as the scientific star of psychoanalytic approaches rapidly waned around the same time.

Edit: There seems to have been some limited attempts to update the theory for modern dynamical systems tools around the turn of the millenium (Kokoszka, 1999; Kokoszka, Bielecki and Holas, 2001), but still nothing empirical to validate it.

References

Kokoszka, A. (1999). Information metabolism as a model of human experiences. International journal of neuroscience, 97(3-4), 169-178.
Kokoszka, A., Bielecki, A., & Holas, P. (2001). Mental organization according to the metabolism of information model and its mathematical description. International Journal of Neuroscience, 107(3-4), 173-184.


Is memory biased towards positive or negative memories? I am trying to understand the relationship between positive/negative memories and the congruence of memory to existing beliefs.  These quotes are from Wikipedia, presented in alphabetical order:

Choice-supportive bias: "positive aspects tend to be remembered as part of the chosen option, whether or not they originally were part of that option, and negative aspects tend to be remembered as part of rejected options."
Egocentric bias: "This bias suggests that people remember the past as
they want it to be rather than the way it was"
Fading affect bias: "a psychological phenomenon in which information
regarding negative emotions tends to be forgotten more quickly than
that associated with pleasant emotions."
Mood congruent memory bias: "the improved recall of information
congruent with one's current mood."
Mnemic neglect: "a pattern of selective forgetting in which certain
autobiographical memories tend to be recalled more easily if they are
consistent with positive self-concept."
Negativity bias: "the psychological phenomenon by which humans have a
greater recall of unpleasant memories compared with positive
memories."
Placement bias: "tendency to remember ourselves to be better than
others at tasks at which we rate ourselves above average and tendency
to remember ourselves to be worse than others at tasks at which we
rate ourselves below average."
Pollyanna principle: "the tendency for people to remember pleasant items more accurately than unpleasant ones."
Positivity effect: "older adults' memories are more likely to consist
of positive than negative information and more likely to be distorted
in a positive direction."
Rosy retrospection: "refers to the finding that subjects later rate
past events more positively than they had actually rated them when
the event occurred"
Self-verification: "self-views bias memory recall to favor
self-confirming material over non-confirming elements."

Most of these suggest congruence with existing beliefs rather than a strict positive bias, but since "on the balance, most people tend to view themselves positively," and most people are happy, it makes sense that there would be a positivity bias overall.

The oddball in the above list is Negativity bias, that appears to contradict other findings.  Another exception is Mnemic neglect: "mnemic neglect is based on self-protection rather than self-verification" - ie, there is a strict positive bias, rather than a congruence with existing beliefs, in direct contradiction with research in Self-verification and others.

I think the resolution of these apparent contradictions is in the details: Is the memory about personal experience or just memorizing items?  Is the memory self-referent or otherwise?  Is the bias referring to memory encoding or memory recall?  Is it an issue of missing or distorted memories?

So my question is, is anyone aware of any studies that look at the circumstances under which memory bias is strictly positive, congruent with existing beliefs, strictly negative, or unaffected by mood or belief?  Or failing that, a comprehensive review of memory bias that might clarify this?

The short answer is: it depends on age. For younger adults, negative memories last longer than positive memories. The opposite is true for older adults (above 60 years old).

This paper is a good review of some of the above effects: Choice-supportive bias, Mood congruent memory bias, Positivity effect, and Negativity bias. It suggests that negative bias only exists among younger adults, while positive memories last longer than negative memories among older adults. The paper also provided several explanations. One of them is that older adults tend to exhibit auto-activation of emotional regulation ability, thus cognitive control comes into play during the memory recall process.

Mather, M. (2006). Why memories may become more positive as people age. Memory and emotion: Interdisciplinary perspectives, 135-158.


What does Inter-Personal conflict means in clinical evaluation? Bob suffers from depression and thinks he has dementia. He goes to see a Psychologist who conducts Rorschach test and gives the following evaluation:

The problem might be because of Inter-Personal Conflict

I am not an expert in Psychology. What does it means and what inference can we draw from it?

A common definition of "conflict" is readily retrievable and applicable in the context of clinical evaluation – i.e., conflict has no particularly unusual primary meaning in clinical psychology. "Interpersonal" also operates as an ordinary adjective with the usual meaning. Thus interpersonal conflict is conflict between persons, as might be distinguished from intrapersonal conflict (e.g., cognitive dissonance). In some cases, one might also distinguish interpersonal conflict from impersonal conflicts with people in general, such as alienation, aggression, or other antisocial impulses when these do not have a specific person or a small group of specific persons as the object of negativity or source of opposition.

Two important inferences that one might consider based on such an evaluation include the plausibility of problems with social skills and problems arising from the other person(s) involved. People who have not developed strong social skills like empathy, conflict resolution, tolerance, or politeness experience interpersonal conflicts more often, but even people with strong social skills and other essentials of psychological health may find themselves at conflict with others who are the primary source of distress or disagreement.


Transsexuality in animals other than humans? In some research papers, transsexuality is correlated with measurable differences in brain structure.  For example:

Zhou et al. (1995) inspected the central subdivision of the bed nucleus of the stria terminalis (BSTc), and found female-sized BSTc's in male-to-female transsexuals.
Berglund et al. (2008) found female-like hypothalamus activation in male-to-female transsexuals in response to smelling odorous steroids.

If there is a neurobiological basis for transsexuality, it seems reasonable to expect to see transsexuality in non-human animals.  This leads me to my question:

Has transsexuality been observed in animals other than humans, and how was it observed?

References:

Zhou et al., A sex difference in the human brain and its relation to transsexuality, Nature 378 (1995), 68-70.
Berglund et al., Male-to-Female Transsexuals Show Sex-Atypical Hypothalamus Activation When Smelling Odorous Steroids, Cereb. Cortex 18 (2008), 1900-1908.

Transexuality is a very social (and human) phenomena that's directly a consequence of how we define it as a society and indirectly a consequence of having distinct male/female ideologies.

Humans can be born as an ambiguous sex.  We have a wide spectrum of hermaphrodites from androgen insensitivity syndrom (i.e. genetically "male" but can be legally "female" and can have varying degrees of both sex organs).  So our definitions of male/female aren't exactly robust in the first place.

Most (probably all) animals do not have language and are unlikely to have social symbols that are meaningful to them.  Most plants can change sex under stress, oysters can, too.  Many organisms don't have a defined sex role (all of them are hermaphrodites).  C. elegans are mostly hermaphrodites but can have the rare male.  Often, the gender changes here are a direct biological response, rather than a social response, whereas with humans, it's more about responding to a social label.

There's some small chance that some other species have developed some sort of social sex expectations (I.e., gender) and have somehow had members challenge it, but it would be really hard to tell without sharing brain architecture, facial expressions, or language with them.


What causes people to feel depressed without there being a problem? I have noticed that some people have lives that appear perfectly fine, yet they feel depressed. In my specific case the feeling typically  lasts for a few days and then magically disappears, only to reappear a couple of weeks later.

In the absence of a real problem (e.g., loss of a close friend, physical sickness, etc), what causes these periods of negative affect?

"Their lives are perfectly fine" is a hard to test thing. Hard to compare. How people feel and respond is deeply contextual.

However there are several potential reasons:

They may be 'wired' to feel stress or respond emotionally (i.e. Due to the way their brain has developed).
A feeling of not being in control (This is often hard to perceive from outside and removed from concrete factors). The causes and triggers of this are varied and complex.
A physical response. e.g. Things like a sensitivity to Gluten can cause incredible changes to our emotions and physiology. Often this manifests in good and bad periods.
Negativity can be a reflection of the context or surroundings. Those same people may appear positive in a different context.
Mental illness can manifest in uneven patterns. This spans from mild (common) to severe symptoms.


Is quantum tunneling required for nerve signals to cross the dendritic synaptic barrier? A person says:

"It turns out that the synaptic barriers of dendrite brain cells are too thick for nerve signals to classically cross. This means that nerve signals need to use Quantum tunneling to cross the dendrite synaptic barrier."

This is supposed to have the consequence that all classical models of the brain are false, and that only quantum based models of consciousness can work for explaining the mind.

Is this true? Is there a way for particles or nerve signals to cross the dendritic synaptic barrier without quantum processes?

I don't know what precisely "nerve signals" is supposed to refer to, but neurons exchange information mainly via one pathway: neurotransmitters. And these do not travel the synaptic cleft via quantum tunnelling - obviously, since quantum tunnelling is a phenomenon on a quantum scale (concerning electrons), while neurotransmitters are far larger, at the molecule level.
There are a number of other ways by which neurons cooperate, such as ephaptic coupling. However, the main one is the release of neurotransmitters following an action potential in the presynaptic neuron. Neurons are connected at their synapses, mostly via axo-dendritic chemical ones. That means that one neuron's axon (its "output line") is met by a part of another neuron's dendrite tree. The point where the two meet is the synapse. Axon and dendrite do not actually touch; there is a microscopic "synaptic cleft" between the two, in which the extracellular fluid which fills the brain flows. I assume it is the synaptic cleft which the "dendritic synaptic barrier" is supposed to refer to.
During the action potential, the presynaptic neuron releases neurotransmitters, such as GABA or Glutamate, into the cleft. These passively diffuse within the cleft, eventually coming in contact with the post-synaptic neuron. There, they bind to receptors which activate the post-synaptic neuron.
As far as I know, neither the release of neurotransmitters at the presynaptic neuron, nor the passive diffusion process through the synaptic cleft, or the binding to postsynaptic receptors require quantum tunnelling to any interesting degree. Basically, the stuff just floats around in the extremely narrow synaptic cleft until it comes across a receptor.
Possibly, the "person" you are talking about means some other aspect of the process, such as the receptor binding. Alas, I do not see how the specific way by which action potentials propagate is relevant for consciousness. Consciousness does not seem to depend on what happens at a specific synapse, but to the large-scale patterns of neuronal activity. If neurons were to communicate via lasers, electrically, or as they do (chemically) hardly seems to matter - what matters is that they communicate, and which neurons communicate, and what they communicate.

All of this are very basic, well-established facts about the workings of the brain. The wikipedia article is a perfectly fine introduction, though literally any neuroscience textbook will explain it like that, and countless research papers in peer-reviewed journals have investigated the process in detail, e.g. this.

There exist a number of theories regarding cognitively relevant quantum phenomena in the brain, most prominently probably Orch OR. As far as I understand it, Orch OR does not focus on the communication between neurons at chemical synapses, but on quantum states within neurons and other forms of coupling (some ephaptic coupling/electrical synapse hybrid?). Regardless of what Orch OR proposes of how the brain works, the chemical synapse is commonly thought to be the primary way by which brain neurons exchange information, and there, neurotransmitters don't tunnel, but diffuse - trivially; since neurotransmitters, being molecules, are far too large to quantum tunnel.
Furthermore, Orch OR is universally assumed to be a rather bad model of the brain.
Certainly, other perspectives exist; but the basic process of action potential propagation via chemical synapses has a well-deserved near dogmatic status in the neurosciences.

Lastly, the person you're quoting seems quite confused about very fundamental brain anatomy. For example, there are no "dendrite brain cells". The brain hosts neurons, each a single cell, each with a dendrite tree (see here for a famous picture). I wouldn't expect anybody who doesn't even understand what a neuron is to revolutionise neuroscience any time soon.


How does the brain act on the information gained via eye saccades? I've often heard that the process of saccading can be described as a statistical sampling technique. Specifically, the standard textbook definition of the function of saccades seems to be that the field of vision is too complexity to known in its entirety, so we look at a representative sample of it in order to form a generally adequate representation.

But this conceit seems to be made purely on a loose analogy to much more well defined problems than vision (e.g. anything soluble via Monte Carlo Method), and in the perception literature I haven't found any proposed mechanisms by which this integration of sampled information could occur.

So my question is this: If eye saccading is best thought of as a sampling process, then how does he brain integrate the sampled information? And if not, then what are some viable alternatives to how the brain makes use of the sequence of images producing via saccading?

A good place to start for a high level understanding of all perception and action is Jaoquin Fuster's perception-action cycle. As he says, it's a "cybernetic cycle linking the organism to its environment". He describes two moieties of the brain, posterior sensation moiety, and the anterior behavioral moiety. Information cycles between perception, interpretation (in the posterior moiety), action plans (in the anterior moiety), and actual movement. The movement is perceived, and the cycle continues. This is a good frame for thinking about how saccades work.

Your actual question then is opening a big ol' meaty can of worms. How the brain makes use of the sequence of images produced by the saccades, is actually two questions. First, how does the brain perceive images? Next, how are saccades relevant to this? In the context of the perception-action cycle, we're then looking at how the posterior moiety interprets visual information, and how the anterior moiety acts on that interpretation. Without writing 10,000 words, I'll try and give a thumbnail sketch of this. Then I'll try and circle it back to answer your specific question.

So, how does the brain interpret visual images? Here we only really need to understand that the posterior moiety creates distributed and hierarchical cell assemblies representing increasingly complex sets of features.  Distributed because the cell assemblies are sparse, as in they consist of many scattered members each representing a different feature. In some way these are bound together to form the gestalt of the object. Hierarchical because cortical regions are connected in a way where successive regions integrate features from previous regions. So, basically a hierarchical set of cell assemblies are activated and thus the sensory information is represented in the mind.

One point before moving on: these cell assemblies are temporal. They represent information over time. It's not so obvious in vision, but for other sensory modalities it is. What does a single configuration of cochlear activations mean? Or a single configuration of touch sensors? Not much. It means vastly more in temporal sequence. A melody, or a hand patting your shoulder. Vision is not different, the confounding thing is that each individual configuration carries so much information it's easy to think of the visual system as a static system. But it isn't. Saccades themselves are helping create temporal information, by focusing on successive things. If you think in terms of the activity of the retina, instead of the static external scene, you'll see that saccades are an integral part of making visual information temporally dynamic.

Because of this, I don't think it is optimal to think of saccades as a procession of images. On the level of the retina, or V1, this might be true. But throughout the perceptual moiety, these images are bound together. Each saccade doesn't present a radically new image, it elaborates an already existing image within the mind. The higher hierarchical regions are binding the information from each saccade into a framework.

Ok, so if the posterior moiety understands the scene, how is it translated into an action (like a saccade)? I believe the answer is the route through the basal ganglia. The basal ganglia helps "select" motor behaviors. To put it very simply, the perceptual moiety is the input, and the output goes to the anterior motor moiety. Through mechanisms that are unclear, a transform is done where a saccade movement is disinhibited that will move the eyes to the bit of the scene that it wants to see next.

I realize I'm shooting kind of wide here, so let me know if you want to know about something more specific. I'm just not sure that your current question can be answered narrowly.

  Fuster, J.M. (1990). Prefrontal cortex and the bridging of temporal
  gaps in the Perception-Action Cycle. Annals of the New York Academy of
  Science, 608, 318-336.

  Felleman, D.J., & Van Essen, D.C. (1991). Distributed Hierarchical
  Processing in the Primate Cerebral Cortex. Cerb Cortex, 1, 1-47.

  Sakurai, Y. (1999). How do cell assemblies encode information in the
  brain? Neuroscience & Biobehavioral Reviews, 23, 785-796.

  Engel, A.K., Konig, P., Kreiter, A., Schillen, T.B., & Singer, W.
  (1992). Temporal coding in the visual cortex: new vistas on
  integration in the nervous system. Trends in Neurosciences, 15,
  218-226.

  Hikosaka, O., Takikawa, Y., & Kawagoe, R. (2000). Role of the basal
  ganglia in the control of purposive saccadic eye movements. Physiol
  Rev, 80, 953-978.


How does the inner ear encode sound intensity? Different areas of the inner ear (the cochlea) are sensitive to different acoustic frequencies. Hence, the cochlea basically performs a fast Fourier transform on the audio signal. This spectral information is subsequently sent to the auditory cortex. But how does the cochlea encodes the intensity of an acoustic stimulus?

Short answer
Hair cells in the cochlea can code sound intensity via the amount of neurotransmitter they release. Higher sound levels result in more neurotransmitter release and in turn to higher firing rates in the spiral ganglion cells of the auditory nerve.

Background
Sound waves are picked up by the mechanoreceptors in the inner ear: the hair cells. Hair cells release the excitatory neurotransmitter glutamate. Dependent on the direction of the deflection of the hairs (stereocilia) on the hair cells, the hair cell releases more neurotransmitter (activation) or less (inhibition) than at its resting state (Fig. 1). The released glutamate activates the primary sensory neurons that connect to the hair cells, namely the spiral ganglion cells (SGCs). The axons of the SGCs combine to form the auditory nerve (Fuchs, 2005).

Fig. 1. Hair cells are activated when their stereocilia are bent in one direction (depolarization) or inhibited when the cilia bend to the other direction (hyperpolarization). source: Yanowski

The hair cell cilia contain mechanoreceptor proteins, that open or close, dependent on the direction in which the cilia bend (Fig. 2).

Fig. 2. Mechanoreceptors in the cochlear hair cell. source: Hudspeth (2014)

Because sound waves have sinusoidal shapes, hair cells undergo cycles of activation and inhibition, closely following the input waves. Louder stimuli cause the cilia to bend further. This causes larger responses in the hair cell and larger amounts of neurotransmitter to be released in the depolarizing phase of the auditory stimulus. This in turn leads to higher spike rates in the spiral ganglion cell axons (Fuchs, 2005). Spike rate in the spiral ganglion cells are thought to primarily encode sound intensity (Heil et al., 2011)

A secondary mechanism of loudness coding may be related to the fact that increased sound levels activate a larger area in the cochlea, due to the low-frequency tail (Kiang & Moxon, 1974). Hence, more neurons start firing at higher sound levels when the tone frequency is the same. However, although it is a plausible mechanism, it is a secondary intensity code, if any.

References
- Fuchs, J Physiol (2005); 566(1): 7–12
- Heil et al., J Neurosci 2011; 31(43): 15424-37
- Hudspeth, Nature Rev Neurosci (2014); 15: 600–14
- Kiang & Moxon, JASA 1954; 55(3): 620-30


How to measure galvanic skin response with wearables? I'm trying to measure galvanic skin response in real-time with a wrist-wearable device, similar to what is being done in the paper "Using Noninvasive Wearable Computers to Recognize Human Emotions from Physiological Signals" which is used the, now discontinued, BodyMedia SenseWear. What solutions exist for this problem? From my preliminary research, I have found:

The Microsoft Band (no longer supported)
The Empatica E4 and Embrace
iMotion GSR
Jawbone UP3 (according to this blog post)

Are there other solutions that I've missed? How does one compare the accuracy of these various solutions?

A system that I am currently testing is the MoviSens EdaMove. The system consists of a small device that can be attached to the arm, and two electrodes to measures EDA at the palms of your hand. The EdaMove uses the exosomatic method, by applying a 0.5V direct current, and samples with 32 Hz. An accelerometer is also included in the sensor, so that you can correct the EDA recordings for movement.

So far, the recordings are pretty good, but I haven't done any formal testing yet. Usability-wise, it may not be the best solution, since it is somewhat more intrusive than a wristband/watch.

Update: This is the fun part. Skin conductance is a measure of skin sweatiness. Unfortunately, the stickers that attach the sensors to the skin (similar to how ECG/EEG-reference sensors are attached) let loose when the hands start to sweat. This is even more so with many movements. For tasks that require much manual work or fine hand-movements, the EdaMove may not be the best sensor.

From the E4, I know that performance is not perfect, but it is okay. Benefit is that the E4 also includes an PPG sensor and accelerometer. Moreover, the E4 allows you to monitor the recordings in real time with their Android/iPhone app.

There are two major issues though with the E4. 1: It needs a good connection with the skin. If not, you could rather easily have missing data (especially so for the HRV sensor). The sensor should thus fit rather tightly. 2: Empatica applies some filtering of the data before you can extract it. It is not clear, however, to what extent it is being filtered. NB. The website states that raw-data is provided. Only the interbeat intervals (IBI), an HRV metric appears to be filtered.


Can someone who is never speaking of himself and present himself as very altruistic be egocentric / narcissistic? I've tried to make some searches on egocentrism and its opposite (Allocentrism).

The definitions from Wikipedia are:

  Egocentrism is the inability to differentiate between self and other.
  More specifically, it is the inability to untangle subjective schemas
  from objective reality; an inability to understand or assume any
  perspective other than their own.

  Although egocentrism and narcissism appear similar, they are not the
  same. A person who is egocentric believes they are the center of
  attention, like a narcissist, but does not receive gratification by
  one's own admiration. An egotist is a person whose ego is greatly
  influenced by the approval of others while a narcissist is not.

  Allocentrism is a collectivistic personality attribute whereby people
  center their attention and actions on other people rather than
  themselves.

But since the prosocial actions are often motivated by ego needs (see Polatch effect for the extreme) can we say that among extreme idealistic people (i.e. militants in extreme organizations) we can find Narcissists as well?

A narcissist has absence of self-compassion, he thinks to be perfect. Is there a correlation between some form of Narcissism and altruism?

EDIT: I found this

  “(The) Israeli zoologist Amotz Zahavi (suggested that) (a)ltruistic
  giving may be an advertisement of dominance and superiority.
  Anthropologists know it as the Potlach Effect ...  Only a genuinely
  superior individual can afford to advertise the fact by means of a
  costly gift ... through costly demonstrations of superiority,
  including ostentatious generosity and public spirited risk taking...
  (I)f Zahavi is right ... conspicuous generosity (is) a way of buying
  unfakeably authentic (self-)advertising.”

(any help at improving the question is very welcome)

According to the empathy-altruism hypothesis, in some circumstances, people help because they genuinely care about the welfare of the other person and not because of any other personal goal i.e. avoid distress, social norm, Self-affirmation etc.

  The empathy-altruism hypothesis basically states that
  psychological altruism does exist and is evoked by the empathic desire
  to help someone who is suffering. Feelings of empathic concern are
  contrasted with feelings of personal distress, which compel people to
  reduce their own unpleasant emotions. People with empathic concern
  help others in distress even when exposure to the situation could be
  easily avoided, whereas those lacking in empathic concern avoid
  helping unless it is difficult or impossible to avoid exposure to
  another's suffering.

...

  The social exchange theory states that altruism does not exist unless
  benefits to the helper outweigh the costs. C. Daniel Batson disagrees.
  He holds that people help others in need out of genuine concern for
  the well-being of the other person. The key ingredient to helping is
  "empathic concern". According to his 'empathy-altruism hypothesis', if
  you feel empathy towards another person you will help them, regardless
  of what you can gain from it (1991).

There is a lot of debate about the empathy-altruism hypothesis theory, but I tend to agree with it.


What causes someone to frequently see particular patterns of digits when they look at a clock? Over the past few years when I randomly choose to look at a clock I typically see particular patterns of times. The main pattern is repeating digits (e.g., 04:04; 11:11; 16:16). This occurs on multiple clock-based devices.

What can explain the tendency to frequently see particular patterns of time when checking the time?

In general humans are excellent at seeing patterns in randomness.
It seems like you have attached special meaning to certain patterns. It seems similar to the way people form superstitions.

Checking the time may also be something that we do so regularly and automatically that we do not know how often we do it. And it may be that the pattern confirming cases rise up and appear to be of significance, whereas the many other non-conforming patterns go unnoticed.

We also have a fairly reasonable internal clock. And people also form habits. So it may also be that you have habituated to checking the time more frequently around these times.


What is the simplest entity that would be considered "conscious"? Generally, we think of humans as having a (relatively) advanced level of consciousness, but we don't think of simple molecules as having any sort of mental capacity at all. So where in between does the phenomenon of consciousness arise?

Update: I have chosen G.Tononi's definition: the quantity of consciousness corresponds to the amount of integrated information generated by a complex of elements

As strange as it may seem the answer to the question is that when two braincells or neurons work together a small conciousness is created. We have billions of neurons so that conciousness would be rather small. Of course, this depends on the definition of counciousness and neurons.


Is rapport a cognitive phenomenon? "Building rapport" is often mentioned as one of the most fundamental sales techniques, but I had a hard time understanding the cognitive mechanism behind this. Is this really a state of awareness that can be analysed via cognitive science tools, or just a salespeople buzzword?

"Building rapport" is not actually A technique, but a general phrase that may cover a whole lot of specific techniques.

"Rapport" does not normally occur in scientific contexts, it mostly occurs within anecdotal subjects like sales and NLP.
Individual sales techniques and NLP is usually not based on science at all, so they do not care for what is scientifically correct or what can be scientifically studied.
"Rapport" consists of several smaller subjects, like trust, various psychological phenomenons, various unconscious processes, emotions, etc etc etc - which are the common phenomenons to refer to in science.
So "rapport" is nothing more than an umbrella term including several phenomenons that are far from restricted to "rapport".
Thus it would not even make sense to study "rapport" specifically.

Also note that sales techniques and NLP tutors like to give their own names on phenomenons and processes that already have a scientific name for them.
I noticed this as I read a book on NLP by Richard Bandler, and this may be another reason why "rapport" has not made its way into science.

The field of "rapport" was never meant to be based on science, and you are not meant to look those things up in science.
This means two things:

Don't expect what you learn about "rapport" to make any sense scientifically, because it's not based on science at all.
If you want to better understand that which is actually supported by science, then you need to search for a more specific phenomenon.


What does double dissociation really tell us? In psychological research, a single dissociation is when a manipulation leaves one cognitive function (say, A) intact whilst severing another (say, B). This indicates the functions A and B are at least partially independent. A double dissociation is when there exists, in addition, a manipulation that does the reverse (i.e. leave B intact whilst severing A). On the Wikipedia page for dissociation in neuropsychology/cognitive neuroscience (I'm assuming the "manipulation" is a brain lesion now) it says that "establishing a single dissociation between two functions provides limited and potentially misleading information, whereas a double dissociation can conclusively demonstrate that the two functions are localized in different areas of the brain." This can't really be true, can it? Consider the following Venn diagram, where the (necessary) neural substrate of A and B are represented, including their intersection:

A double dissociation could consist of a manipulation in A \ B and another in B \ A. The functions would still be partially dependent, however, and not localized in completely different areas of the brain. So, in effect, the only thing a single dissociation proves is that the circles for A and B are not identical, and the only thing a double dissociation proves (in addition to the fact that they're not identical) is that one is not a subset of the other. Is that about right?

Double dissociation does not prove the independence of certain cognitive functions and their neural substrates. What it does is provide stronger evidence for which the best explanation is the independence of certain neurocognitive systems.
The brain is on many aspects not a marvel of engineering with many areas being responsible for a spectrum of functions and behaviours or for different aspects of a seemingly unitary cognitive faculty. On top of that, it is often difficult to make a proper classification and distinction between certain functions and behaviours (examples are episodic/semantic memory and perceptual/semantic priming) which, in many cases, limits the validity of the conclusions drawn.

So I don't know if a "conclusive demonstration" is possible. However, under properly defined terms, a double dissociation can provide strong support for independence with little possibility of an intersection between neurocognitive systems because if an intersection existed, it would be highly possible for a function to be retained at some level even after the hypothetical brain system responsible for it, suffers a lesion.


Why is working memory so small? I know that the concept of working memory may be subject to discussion. Still, there is a storage capacity limit. This is a real mystery to me. Working memory is known to be positively correlated to various tests (IQ for example). Why did natural selection not grant us a better storage capacity?

Before asking this question, I read some hypotheses by Cowan: The Magical Mystery Four: How is Working Memory Capacity Limited, and Why?
Two camps are presented: capacity-limit-as-weakness and capacity-limit-as-strength.
Basically the first camp explains this weakness from a neuronal point of view, claiming that keeping many items active is greedy and can cause interference. The second camp pretends that the lesser the number of items accessible is the quicker the cognitive processes are (chunking, searching, etc.). Honestly I don't know what to think. More than that, I don't feel its very convincing. If our neural system has evolved toward some incredibly powerful processing modules and can't even keep 10 items active at the same time, there must be a reason. I am more inclined to think that the capacity limit is a kind of strength somewhere, but I don't feel very convinced by the examples provided in the short passage I mentioned.

Do you have any extra arguments for/against any of these theoretical positions?
My preconception is that this limit constrains us to encode the real in the most powerful fashion. In short, we are always forced to learn more complex patterns. Is it relevant or not? Do you have any source which could challenge or back up this view?

There's a huge amount of perspectives you could take in answering a question like this, but I would like to approach it from the perspective of dual process theories (see the Evans, 2008 Annual Review paper for an outline). I'm not going to reference this answer much beyond that, because almost all the information is adapted from this review, with some explanation.

There's any number of specific dual process theories, but they all state that cognition is divided between type 1 processes, which are fast, parallel, automatic, implicit, and generally don't vary between people, and type 2 processes, which are slow, serial, controlled, explicit, and crucially, rely on working memory.

The evolutionary side to this is type 1 processes are the specialized, domain specific evolved functions of our brain to deal with specific problems, like predicting the destination of moving objects, recognising faces, or figuring out how similar lions are to tigers. Type 2 processes (i.e. working memory), on the other hand, are domain general, in that they can be flexibly applied to any domain, rather than just the task they evolved to solve, but this flexibility comes at cost of limited capacity, increased mental effort, and so slower processing.

This limitation is referred to in the dual process literature as 'the singularity principle' (Evans, 2006) - system one, by processing in parallel, can deal with an incredible amount of information at the same time (and needs to, because it takes care of the basic functions that keep us alive from day to day), while the slower type 2 processes can only actively process one piece of information at a time (but can keep "7 plus or minus 2" "chunks" of information in mind if they don't have to be manipulated; Miller, 1956).

...By analogy, think of the difference between the old-fashioned telephone in your house, which was designed for only one function, and so performs it perfectly, with minimal resources, and a smartphone, which can theoretically perform any computational or communicative function, but occasionally disconnects your calls for no apparent reason.

Some References

Evans, J. S. B. (2008). Dual-processing accounts of reasoning, judgment, and social cognition. Annu. Rev. Psychol., 59, 255-278.

Evans, J. S. B. (2008). Dual-processing accounts of reasoning, judgment, and social cognition. Annu. Rev. Psychol., 59, 255-278.

Miller, G. A. (1956). The magical number seven, plus or minus two: some limits on our capacity for processing information. Psychological review, 63(2), 81.


In general, how does one resolve two competing theories in Psychology? In looking at a post on twitter from a somewhat well-known psychologist Tal Yarkoni, he references a paper which lists multiple sets of competing theories in Psychology that have not been resolved.

This is interesting to me and related to my question on selecting "the most well supported" among competing theories of generalized anxiety disorder (link).  But, I could see this being related in other areas, such as procrastination research where psychologists with different focuses explain the phenomena differently (as elaborated in this video.)

As an aspiring research scientist, I am curious what it takes today to resolve competing theories in Psychological science?  I read that it may take a joint research paper between the authors of the differing theories with conditions of what defines sufficient evidence, but certainly there must be another way, because some authors may be deceased, unavailable, etc.

Moreover, why might these disputations, it seems like there are 13 of them (26 theories in total), some dating back to the 50s, still be unresolved today?

I think this question should be germane to the topic, because in a meta post here, the moderator agrees that meta-science posts are fair questions for this site.

Almost every pair of theories on that list sets up a false dichotomy.

It is not an issue of one theory over another; at issue is how much different explanations apply to different circumstances. There is at least some evidence for each possibility that is not explained away by the other.

Resolving these dichotomies in favor of one theory or the other is probably not a worthwhile pursuit.

However, many papers are published that are greatly informative on some of these issues, and in fact if you had scrolled down just a bit on your own link or followed up a bit, you would find that the original author of the table presented in that tweet has an updated list (though several years old now) that mentions several such papers: https://faculty.washington.edu/agg/pdf/PPS_2012_supplement.Unresolved_controversies.pdf

I especially like this footnote from that link, which I think strongly supports my answer (emphasis mine):

  b This controversy is treated as unresolved by some researchers, but the recent article by Smith
  and Grossman (2008) has argued, using brain imaging evidence, for “multiple systems of category
  learning”, which suggests a controversy resolution in the form treating multiple theories of the nature of
  category representations as valid in distinguishable domains of application.

So to answer your question:

  In general, how does one resolve two competing theories in Psychology?

In general, one resolves the existence of competing theories by testing cases where one theory or the other better explains an experimental result and attempts to resolve the conflict by finding mediating factors that prefer one theory over the other (or some entirely separate theory that may explain all or part of the data).

This is usually an incremental, iterative process, not something that is resolved in one key work.

References

Greenwald, A. G. (2012). There is nothing so theoretical as a good method. Perspectives on Psychological Science, 7(2), 99-108.