Probiotics and Mental Health While trying to find research articles within the realm of Psychosynthesis, I have been looking at the "collective unconscious"

Image Source: Wikipedia Commons - (CC BY-SA 3.0)

Lower Unconscious
Middle Unconscious
Higher Unconscious
Field of Consciousness
Conscious Self or "I"
Higher Self
Collective Unconscious

Conducting a Google Scholar search for "collective unconscious" I stumbled on an article by Dinan, et al. (2015) which states:

  Gut microbes are part of the unconscious system influencing behavior.
  Microbes majorly impact on cognitive function and fundamental behavior patterns.
  Disorganisation of the gut microbiota can negatively impact on mental health.
  Psychobiotics are probiotics with a potential mental health benefit.

they also talk about bidirectional communication between gut microbes and the brain occuring via a number of routes including the vagus nerve (cranial nerve X), the hypothalamic-pituitary-adrenal axis (HPA) and cytokines produced by the immune system.

  Bacteria also have the capacity to generate many neurotransmitters and neuromodulators. For example, certain Lactobacillus and Bifidobacterium species produce gamma-aminobutyric acid (GABA); Escherichia, Bacillus and Saccharomyces spp. produce norepinephrine (NE); Candida, Streptococcus, Escherichia and Enterococcus spp. produce 5HT; Bacillus produces dopamine (DA); and Lactobacillus produces acetylcholine (Lyte, 2011, Lyte, 2013, Wikoff et al., 2009). Some probiotics can modulate the concentrations of opioid and cannabinoid receptors in the gut epithelium (Rousseaux et al., 2007). However, how this local effect occurs or translates to the anti-nociceptive effects seen in animal models of visceral pain is currently unclear.

My question is can poor mental health affect the bidirectional communication between gut microbes and the brain, and can consuming products containing probiotics be used to help with mental health problems?  If so, will consuming products containing probiotics when well cause mental health problems?

References

Dinan, T. G., Stilling, R. M., Stanton, C., & Cryan, J. F. (2015). Collective unconscious: how gut microbes shape human behavior. Journal of psychiatric research, 63, 1-9.DOI: 10.1016/j.jpsychires.2015.02.021

Lyte, M. (2011). Probiotics function mechanistically as delivery vehicles for neuroactive compounds: microbial endocrinology in the design and use of probiotics. Bioessays, 33(8), 574-581.DOI: 10.1002/bies.201100024 Free PDF: Semantic Scholar

Lyte, M. (2013). Microbial endocrinology in the microbiome-gut-brain axis: how bacterial production and utilization of neurochemicals influence behavior. PLoS pathogens, 9(11), e1003726.DOI: 10.1371/journal.ppat.1003726

Rousseaux, C., Thuru, X., Gelot, A., Barnich, N., Neut, C., Dubuquoy, L., ... & Ouwehand, A. (2007). Lactobacillus acidophilus modulates intestinal pain and induces opioid and cannabinoid receptors. Nature medicine, 13(1), 35.DOI: 10.1038/nm1521

Wikoff, W. R., Anfora, A. T., Liu, J., Schultz, P. G., Lesley, S. A., Peters, E. C., & Siuzdak, G. (2009). Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Proceedings of the national academy of sciences, 106(10), 3698-3703.DOI: 10.1073/pnas.0812874106

The following, and more, is available at my blog article Microbiome and Probiotics: Gut bacteria can affect your mental health?
Answer to Question 1:

Can poor mental health affect the bidirectional communication between gut microbes and the brain?

Even though there is cross talk between your enteric nervous system (ENS) and your brain, researchers assumed that microbes did not play into it. But recent breakthroughs are challenging that assumption, and changing our understanding of how the blood brain barrier works, because the microbiome can affect your brain in some pretty big ways.
The ENS is a massive web spread over your entire digestive tract made up of more than 500 million neurons that control your guts. This second brain as it is sometimes called, is pretty much self sufficient, and can take care of most of its jobs by itself. But it is connected to the CNS through your vagus nerve, which is an information superhighway between your gut and your brain.
Stress affects your microbiome
Early research starting in the 1970s (Tannock & Savage, 1974) showed that stress could affect the kind of microbes found in the guts of mice. One group found that stressing mice by depriving them of food or water, caused them to have more coliform bacteria like E.coli, and less of another form of bacteria called lactobacilli in their intestines.
Another group found that the stress of dealing with an aggressive cage mate led to changes in amounts of other kinds of bacteria. They found increased numbers of Bacteriodes and Clostridium, along with decreased numbers of Coprococcus, Pseudobutyrivibrio and Dorea.
But even though it was clear that stress could affect the kinds of microbes in the intestines, it wasn’t clear if that was a 2 way relationship.
Could Gut microbes be affecting psychological stress levels?
The first big break on this question came when some scientists from Kyushu University, Japan (Sudo, et al. 2004), discovered that exposure to certain kinds of microbes had dramatic effects on brain chemical levels.
For this study, the scientists used germ free mice. These were mice delivered by C section and immediately put into super clean cages, so they were barely exposed to microbes at all. They also made comparisons with specific pathogen free mice. These were mice only exposed to a known set of microbes.
The germ free mice got a lot more stressed when they were restrained, so it was something about the bacteria in the specific pathogen free mice that was helping them with their stress levels.
The team found that the germ free mice had less of a protein called Brain-derived neurotrophic factor (BDNF). BDNF is important for learning, memory, and higher order thinking. The germ free mice had less of it in the brain regions that determine how an animal reacts to stress.
Answer to Question 2 and 3:

Can consuming products containing probiotics be used to help with mental health problems? If so, can consuming products containing probiotics when well cause mental health problems?

There is not a lot of research that is very clear on the relationship between the gut and the brain in humans. These discoveries are so new that nobody has been able to do any large scale studies in humans yet. But along with prebiotics (fibre suppliments designed to feed good bacteria), small studies have tried treating volunteers with probiotics, deliberately introducing new microbes in to there guts, and the microbes and fibre affected the subjects mood and cognition.
So there might be a relationship between your microbiome and your mental health. But the studies have not been able to look closely enough at what exactly the prebiotics and probiotics are doing to the microbes in the gut, or how that may be translating in to changes in mood.
What does this mean?
Researchers will be getting more into the nitty gritty of these relationships and trying to work out whether these discoveries can translate into medical treatments.
Other scientists are trying to work out how to humanize the mouse microbiome, making the mouse microbiome more human like. They are doing this by taking faecal matter from sick and healthy human patients and inserting them into mice to study the effects.
That kind of experiment can let researcher pick apart how differences in the microbiomes connects with changes in mental health. They can also get right into the brains of mice in ways they can’t with human patients, using dissected tissues to look directly at the structures of brain cells and how they connect.
Can we tailor our microbiome for maximum benefit?
Some researchers are also trying to figure out how specific kinds of microbes are affecting our brains and how we can tailor our microbiomes to maximize the health benefits.
Others are starting to ask questions about how other things that affect our microbiomes like antibiotics could be affecting our mental health and cognition.
So there is still a lot we don’t know about how our microbiome can affect our brain. But there are a lot of new studies in the works and scientists and doctors are hoping that as our knowledge of how our Brain-Gut-Microbiome Axis grows, so will our ability to tweak it and hopefully improve some lives along the way.
Further Reading
Bailey, M. T., Dowd, S. E., Galley, J. D., Hufnagle, A. R., Allen, R. G., & Lyte, M. (2011). Exposure to a social stressor alters the structure of the intestinal microbiota: implications for stressor-induced immunomodulation. Brain, behavior, and immunity, 25(3), 397–407. doi: 10.1016/j.bbi.2010.10.023 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039072/pdf/nihms253984.pdf
Bercik, P., Denou, E., Collins, J., Jackson, W., Lu, J., Jury, J., … & Verdu, E. F. (2011). The intestinal microbiota affect central levels of brain-derived neurotropic factor and behavior in mice. Gastroenterology, 141(2), 599-609. doi: 10.1053/j.gastro.2011.04.052 Free PDF: https://www.gastrojournal.org/article/S0016-5085(11)00607-X/pdf
Carabotti, M., Scirocco, A., Maselli, M. A., & Severi, C. (2015). The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Annals of gastroenterology, 28(2), 203–209. pmcid: PMC4367209 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/pdf/AnnGastroenterol-28-203.pdf
Furness J.B., Callaghan B.P., Rivera L.R., Cho HJ. (2014) The Enteric Nervous System and Gastrointestinal Innervation: Integrated Local and Central Control. In: Lyte M., Cryan J. (eds) Microbial Endocrinology: The Microbiota-Gut-Brain Axis in Health and Disease. Advances in Experimental Medicine and Biology, vol 817. New York, NY: Springer. doi: 10.1007/978-1-4939-0897-4_3
Human Microbiome Project Consortium (2012). Structure, function and diversity of the healthy human microbiome. Nature, 486(7402), 207–214. doi: 10.1038/nature11234 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564958/pdf/nihms378076.pdf
Mayer, E. A., Knight, R., Mazmanian, S. K., Cryan, J. F., & Tillisch, K. (2014). Gut microbes and the brain: paradigm shift in neuroscience. The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(46), 15490–15496. doi: 10.1523/JNEUROSCI.3299-14.2014 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4228144/pdf/zns15490.pdf
Mayer, E. A., Tillisch, K., & Gupta, A. (2015). Gut/brain axis and the microbiota. The Journal of clinical investigation, 125(3), 926–938. doi: 10.1172/JCI76304 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4362231/pdf/JCI76304.pdf
Reardon, S. (2014). Gut–brain link grabs neuroscientists. Nature News, 515(7526), 175. doi: 10.1038/515175a Free PDF: https://www.nature.com/news/polopoly_fs/1.16316!/menu/main/topColumns/topLeftColumn/pdf/515175a.pdf
Smith, P. A. (2015). The tantalizing links between gut microbes and the brain. Nature News, 526(7573), 312. doi: 10.1038/526312a Free PDF: https://www.nature.com/news/polopoly_fs/1.18557!/menu/main/topColumns/topLeftColumn/pdf/526312a%20corrected.pdf
References
Sudo, N., Chida, Y., Aiba, Y., Sonoda, J., Oyama, N., Yu, X. N., … Koga, Y. (2004). Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice. The Journal of physiology, 558(Pt 1), 263–275. doi: 10.1113/jphysiol.2004.063388 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664925/pdf/tjp0558-0263.pdf
Tannock, G. W., & Savage, D. C. (1974). Influences of dietary and environmental stress on microbial populations in the murine gastrointestinal tract. Infection and immunity, 9(3), 591–598. pmcid: PMC414848 Free PDF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC414848/pdf/iai00243-0111.pdf


is the mind independent of the brain? or the mind is a mere collection of memories, experiences stored in the brain?

Of course the mind is not independent of the brain.  Otherwise, nobody would do recreational drugs, psychiatric drugs would be useless, and our whole theory of light and color perception, sound perception, and every other sensory perception would be useless and make no predictions.  All of these things tell us how signal in the environment are transduced into electrical signals and processed in the brain.  And while we don't know exactly how it becomes a mental experience (The Hard Problem), we know that there are many direct relationships between activity in the brain and perceptions and states in the mind.

The mind isn't just memories and experiences stored in the brain though, it's also active processing of current stimuli, which includes spontaneous activity that may randomly draw on memories and experiences, but not in a sensible or meaningful way.  That is to say, there are biological processes that aren't really necessary to brain/mind, but to metabolism or long-term evolutionary benefit, yet they still influence brain/mind and we sometimes ascribe meaning to them without merit.


What physical process governs which details are retained in memory? With long term memory, there is loss of information. For example, we don't seem to retain all the details of every image we see. What is the physical process those details undergo which cause them to be retained over the ones that are not, and what is the mechanism that "chooses" which information undergoes that process?

I think this question is not getting answered because it suggests a misunderstanding or lack of understanding about all the forces leading up to your specific question about long term memory. For instance, you imply that we see images in detail to begin with—or that we are able to 'store' a detailed image in short term memory... and that detail simply does not get transferred to long-term memory.

Obviously, humans are still far off from fully understanding how memory functions. We can make some statements about your question now, though. To begin, when we see images, we are not seeing everything—we are only seeing precisely what we are looking at (or focusing on), then our brain is filling in the rest of the information. We think that we see the world pretty clearly; however, this is a combination of our brains ability to fill in missing information with what it expects, and our eyes' ability to rapidly scan its environment—quickly changing focus in order to paint your world (see: saccadic eye movements).

These images, that are intimately connected with the other senses and emotions which are firing at the same time in the brain, are dull from the start. The vividity with which we can recall these images can be considered a function of how impactful the event was on our lives. Like all functions in our bodies, long-term memory is a product of evolution. This implies a likelihood the moments which are most important to remember for our survival and procreation are the ones we can recall most vividly. Did you almost die? Was it your first kiss? Additionally, especially novel moments are remembered well. Were you at the beach for the first time, never having smelled the salt air before?

Moving beyond the question of the vividness of long term memory, we may consider the notion that are long-term memories are actually mutable. Each moment of recall is a moment of re-storing that memory; it is like copying a copy.


Are there cases of drug addict that "forget" their addiction after some brain damages? I'm interested in what I naively call  "memory of addiction" - i.e. the brain restructuration that drugs addicts have and which causes the addict to need more and more to be satisfied.
Then, knowing that some brain accident can cause amnesia, I wondered if there were cases of people who were drug addicts that "forgot" or lost there addiction after some accident (shock, stroke or whatever...).
If you had any report paper on the subject, I'd be glad to know.

I'm not aware of truly "forgetting" as in amnesia, but there have been reports that brain damage can disrupt the behavioral pattern of addiction which I think qualifies as what you describe as what "causes the addict to need more and more to be satisfied".
Naqvi et al 2007 reported that:

smokers
with brain damage involving the insula, a region implicated in conscious urges, were more likely
than smokers with brain damage not involving the insula to undergo a disruption of smoking
addiction, characterized by the ability to quit smoking easily, immediately, without relapse, and
without persistence of the urge to smoke

Patients in this study had damage from either stroke or from surgical resections for cancer or epilepsy.
Naqvi, N. H., Rudrauf, D., Damasio, H., & Bechara, A. (2007). Damage to the insula disrupts addiction to cigarette smoking. Science, 315(5811), 531-534.
See also this review:
Droutman, V., Read, S. J., & Bechara, A. (2015). Revisiting the role of the insula in addiction. Trends in cognitive sciences, 19(7), 414-420.
However, I'd note that brain damage studies like these are quite complicated because damage to one area is often accompanied by other damage, and few subjects have similar lesions, so I'd be more hesitant than some of these authors are to implicate the insula specifically. Notably, the insula is near subcortical structures and fibers of passage that could also be involved.

Stelten, et al 2008 is a review of neurosurgical attempts to target addiction. These are mostly case studies/series and involved complex cases typically with multiple co-occurring psychiatric conditions. The authors raise ethical concerns with some of the studies, as well, including issues of consent and the permanence of interventions and the lack of control comparisons.
Stelten, B. M., Noblesse, L. H., Ackermans, L., Temel, Y., & Visser-Vandewalle, V. (2008). The neurosurgical treatment of addiction. Neurosurgical focus, 25(1), E5.
You can also find more recent papers and reviews that cite this one on Google Scholar which might be a good place to continue your literature search.


What's the difference between simultanagnosia and neurological extinction? Both of these terms describe the inability to perceive more than one object at a time. I'm not too sure what the big difference is between them. Note that I'm referring to 'extinction' as used in neurology (wiki article), and not as used in psychology.

In extinction the patient may be able to get attention to an object in the contralesional field if it is the only salient object. If there is a competition from another object the patient won't draw attention toward the contralesional field (opposite side of the lesion; generally right parietal lobe).

Simultagnosia is described as the inability to perceive more than one object at a time in each visual field. It is consequence of bilateral damage to the parietal lobe

References

E. Bruce Goldstein-Sensation and Perception-Wadsworth (2010)


Can one become addicted to learning? Is it possibly to become addicted to learning?

What drives this addiction and how can it be controlled?

Note:
I'm not sure this is the right exchange for this question... Its the best fit as far as I can see though.

Any form of excessive secretion of dopamine, can not be good, be it drugs, learning, sex etc. workaholism is a form learning addiction,  workaholism is said to be as an addiction
very similar to alcoholism. Workaholic as a “person whose pleasure from learning things at work has become so extreme, that it indicates clear disturbances with his/her personal happiness, bodily health, and interpersonal relations, and with his smooth social functioning” . Therefore,  there are some perspectives related to workaholism. workaholism at least initially was formulated to be referred as addictive process (Sussman, 2012).
 Negative side effects of workaholism or the strive or need to constantly work towards gaining knowledge may include subjective emotional sorrow or feeling of “burned out” (Sussman, 2012).

Based on that search,
these authors induced that addiction includes:
(a) engagement in the behavior to achieve
appetitive effects
 (b) preoccupation with the behavior
(c) temporary satiation
 (d)loss of control
 (e) suffering negative consequences
hope my answer helped. if you want to read in depth on this. do refer to the reference for article.
reference :  Sussman, S. (2012). Workaholism: A Review. Journal Of Addiction Research & Therapy. doi: 10.4172/2155-6105.s6-001


Recording motor-evoked potentials (MEPs) in response to transcranial direct current stimulation (tDCS)? The amplitudes of motor-evoked potentials (MEPs) are often recorded as a measure of (change in) cortical excitability, after administering some form of non-invasive brain stimulation (NIBS). In a typical scenario, magnetic stimulation (TMS) is used to deliver pulses to the motor cortex, and MEPs are recorded from e.g. the index finger.

It has never been clear to me why MEPs can not also be recorded in response to other forms of NIBS that also modulate cortical excitability, most notably electrical stimulation (tDCS). This paper seems to state this axiomatically, without really giving a reason:

  Compared with tDCS, TMS provides a better spatial resolution; when
  used over the motor cortex, it also allows the quantiﬁcation of
  motor-evoked potentials (MEPs), a measure of the excitability of the
  motor system, which tDCS does not.

Any thoughts as to why it is that MEPs are not also prompted by tDCS?

Compared to TMS which is usually brief and high-intensity, tDCS stimulation protocols are fairly weak and long-duration. This protocol doesn't elicit MEPs by itself, because you need a stronger stimulus.

In some studies (see references below), tDCS has been shown to modulate MEPs, but it is probed by using TMS to elicit the MEP, and comparing the evoked MEPs with and without tDCS.

The mechanistic idea is that tDCS is modulating neuronal thresholds, but you still need some sort of a "kick" to actually evoke a MEP.

Nitsche, M. A., & Paulus, W. (2000). Excitability changes induced in the human motor cortex by weak transcranial direct current stimulation. The Journal of physiology, 527(3), 633-639.

Nitsche, M. A., & Paulus, W. (2001). Sustained excitability elevations induced by transcranial DC motor cortex stimulation in humans. Neurology, 57(10), 1899-1901.

Nitsche, M. A., Fricke, K., Henschke, U., Schlitterlau, A., Liebetanz, D., Lang, N., ... & Paulus, W. (2003). Pharmacological modulation of cortical excitability shifts induced by transcranial direct current stimulation in humans. The Journal of physiology, 553(1), 293-301.


What causes the sensation of taste when Dimethyl Sulfoxide (DMSO) is absorbed through the skin? The Wikipedia page for DMSO says:

  The perceived garlic taste upon skin contact with DMSO may be due to
  nonolfactory activation of TRPA1 receptors in trigeminal ganglia

...and references a PLOS1 paper. That paper doesn't seem to address the topic of DMSO taste directly. My understanding is that taste is conveyed mainly through the facial and glossopharyngeal nerves, and the trigeminal nerve conveys sensation/temperature. The paper doesn't seem to explain how a nerve whose activity normally registers as sensation/temperature becomes interpreted instead as taste.

Short answer
It may not be so much the direct action of DMSO on the olfactory sensory system, but the smell of one of its metabolites that is excreted via the pulmonary system and the skin after ingestion of DMSO.

Background
Dimethyl sulfoxide (DMSO) is metabolized in man by oxidation to dimethyl sulfone (MSM) or by reduction to dimethyl sulfide (DMS) (Fig. 1).

Fig. 1. The reaction of DMSO to DMS catalyzed by DMSO reductase. source: wikipedia

DMS is eliminated through the breath and skin and is responsible for the characteristic garlic-like odor of the breath, and taste in the mouth associated with ingestion of DMSO. These effects can become noticeable minutes after ingestion and may last for several hours (Santos et al, 2003).

Reference
- Santos et al., Biochem Pharmacol (2003); 65: 1035-41


What are some theories or cognitive models of human imagination? What cognitive models of human imagination exist? How does the human imagine things that don't exist?

Suppose I ask anyone to imagine himself climbing a mountain. He can't imagine that until he has some experience about mountaineering whether through a movie, documentary or some reading material and Wikipedia page on Imagination says that

  ...without knowledge, imagination can not be developed...

If he has this experience he would be able to imagine himself climbing a mountain. Are there any theories that explain this?

Assuming imagination can be roughly defined as "taking things from reality/experience and mixing them up somehow to create something dissimilar from the inputs", then any cognitive framework:

with a probabilistic interpretation
who is capable of analogy

roughly models how imagination may manifest itself in the human mind.

Imagination as inference

Imagine you've ridden two bicycles: a fast bicycle and a slow bicycle. The bicycle salesman now shows you a third bicycle with a speed in between the two you've previously ridden. Although you do not have any direct experience with the bicycle, you can infer from your two previous experiences that the bicycle will give you an experience somewhere in between the two. This is what I mean by "probabilistic interpretation". If your cognitive model has a concept of a distribution of possible bicycle speeds, it can infer points along that distribution. This approach is used in cognitive models like neural networks.

Imagination as analogy

Consider the analogy:

  Structure of an atom is like a solar system. Nucleus is the sun and
  electrons are the planets revolving around their sun.

Given basic knowledge of the solar system, despite never seeing atoms, you can imagine a few things about atom structure. You can imagine electrons float freely around the center of the nucleus without slowing down. You were able to combine a symbol you had for the solar system with the unknown symbols of electrons and nuclei. This type of imagination is found in cognitive models like ACT-R.

Imagination as something more complicated

The two previous forms of imagination were pretty simple in terms of interactions. Two inputs formed a novel output, but scientists have all sort of theories about how we build models in our heads that involve scaling up to more than one input, drawing experiences from memory and interacting with the environment. There are so many that you have to start developing criteria for what the best model of imagination is. Obviously, I can't cover all the models, but hopefully this gives you a good starting point.


Perceive person's importance to the education Can we perceive, through some indications, if a person gives too much or too little importance to the education and intellectual formation?
Discussing this with some colleagues who say that no because knowledge and its importance are not reflected in behavior. Still, I'm inclined to think that based on some evidenced characteristics, we can assess the value given to knowledge.

I think this issue touches on a number of aspects like self-worth, self-image and self-concept among others.
Undoubtedly people can place a distorted or disproportionate value on self and others based on education. It's mostly a problem of reference, how exactly do you value education and knowledge correctly?

Can we perceive, through some indications, if a person gives too much or too little importance to the education and intellectual formation?

Certainly, if the value they place on education/formation does not correspond to real tangible values. For example the janitor who thinks himself overall more qualified than the brain surgeon. Or the brain surgeon who thinks himself necessarily superior to others in areas where he has no expertise.

knowledge and its importance are not reflected in behavior

This is objectively wrong, for example the study of morals and ethics enables a person to positively change their behavior (as can the knowledge of healthy eating help to change dietary habits.) However, there's no necessary causal relation between knowledge and behavior.


How does ethnic identity contribute to a person's self esteem The process of ethnic identity development is similar to the process of identity development in general. Often the precipitating event involves an experience during which the individual encounters prejudice and becomes aware of his or her group's under-representation in some activity or setting. Following this crisis, individuals engage in a period of exploration during which they immerse themselves about their ethnic heritage. I am interested in knowing more about how this process of self-exploration leads to increases in self-esteem?

I would look at Jennifer Crocker and Brenda Major's paper in 1989, Psychological Review, entitled "Social Stigma and Self-Esteem: The Self-Protective Properties of Stigma" which focuses on how being the target of social stigma can actually be protective of one's self-esteem.  It's not precisely what you're discussing but it comes the closest in the literature I know and they're discussion and bibliography would likely be a good starting point.  Hope this helps!


How did Fechner justify the assumption that the just-noticeable-difference in sensation is constant? As stated here on Wikipedia: 1

Weber's law states that the-just-noticeable-difference (JND) of an intensity of a stimuli divided by the intensity of that stimuli is always constant.

Mathematically: $\Delta(I)/I=Constant$

... where $I$ here means the physical intensity of sound, light and so on.  $\Delta(I)$ is the-just-noticeable-difference.

Then came Fechner and assumed that the-just-noticeable-difference "in sensation" of a stimuli is constant as well, hence: $\Delta(I)/I = Constant = \Delta(S)$

$\Delta(S)$ stands for the-just-noticeable-difference "in sensation."

On what basis was Fechner justified in assuming that the-just-noticeable-difference in sensation is constant?

It was not an assumption; it was a decision. It allowed for better quantification, it gave an operational definition in increase in sensation, which allowed for more common ground in research between different labs. In a way, it's a definition by pure counting: when the subject feels a change in sensation, add one. Then this absolute scale is plotted against the ratio scale of increase in stimulation.


What works for procrastination? Procrastination seems universal and well understood by the public. However, there seems to be very little research into techniques and approaches that works to reduce and manage procrastination.

The previous aversion therapy thread cited a 2012 review that found minimal research into procrastination. It is 2019 now and I was wondering whether anyone knows of any recent research? - Effectiveness of aversion therapy for procrastination

Another thread will address procrastination in ADHD - Treatment and strategies for procrastination for ADHD

I found this 2018 meta-analysis of 24 studies by Wendelienvan & Klingsieck on procrastination intervention - Educational Research Review article.

They used Steel's 2007 definition of procrastination as an irrational and acratic behavior. Procrastination is a voluntary delay an intended course of action despite expecting to be worse off for the delay. Wendelienvan & Klingsieck found that cognitive-behavioural therapeutic approaches had a greater reduction in procrastination than self-regulation and strength & assertiveness training interventions.

Quite an accessible and interesting read.


What is the rationale for the normal distribution of intelligence? What is the rationale for the normal distribution of intelligence?

I'm asking what the rationale is for saying that 68% of variance within intelligence falls within 1 standard deviation either side of the mean, and 95% within 2, etc.. That's just what "normal distribution" means. Here is a picture:

Why not suppose that intelligence is e.g. a uniform distribution? You can see clearly, in the picture below, that if it's modeled in that way:

someone's deviation from the mean will be equal to the probability of their score.

Short answer
IQ scores are distributed normally, because they follow the  central limit theorem.

Background
When we measure IQ scores in sufficiently large populations, they will be normally distributed. This holds for healthy controls, as well as groups of people with ADHD or reading disabilities (Kaplan et al., 2000), and also in people with mild to moderate mental retardation (Bellugi et al. (2003).

Many biological variables follow a normal distribution quite well. This is a result of the central limit theorem, which says that when you take a large number of random numbers, the means of those numbers are approximately normally distributed (McDonald, 2012). When for example the weight distribution is sampled in a population, it will vary with age, nutrition, disease status etc. The addition of these independent random variables result in the variable (in this case weight) to become normally distributed ("bell shaped"), even if the original variables themselves are not normally distributed (source: wikipedia).

Hence, your statement Do we as a society have the right attitude to variation in human intelligence? Because it seems to me we are either over-nurturing the extremes, or should not represent it as a normal distribution doesn't really apply here, as IQ score distributions have nothing to do with 'us as a society having the right to do something'.

References
- Bellugi et al., Enfance (2003); 3(55): 237-49
- Kaplan et al., J Learning Disabilities (2000); 33(5): 425-32
- McDonald, Handbook of Biological Statistics, 3rd ed. (2012). Sparky House Publishing, Baltimore, Maryland


How to address a narcissist to go to therapy? Often people go to a therapist when they start to experience a strong personal discomfort, however often this never happens as because their personality is egosyntonic.

However for whoever is standing near to those persons the situation can become very annoying  (see Does neuroticism cause people to hurt others?).

The narcissist is often unconscious to have a "problem", he simply thinks that the problem comes from others and that his way of thinking should be taken also by others.

How to address a narcissist toward going to therapy?

The person prolly isn't a clinical narcissists only a psychologist could diagnose as such. When you do find one though it's a very tough case.

To be honest one of my current psychologist and I discussed the situation of narcissist therapy in detail. I dated someone who fell somewhere in the empathy disorder spectrum. The person wanted me to announce them to the world and due to my socio-economic situation it would result in what little family I have left disowning me. In general psychotherapy can teach someone who is thus sick how to behave in a manner consistent with the norms of society but there remains some question of current methods ability to remedy the disorder in a way that the changes cause the universe which that person experiences not to revolve around them.

I suggest an appeal to ego might work. My appeals to morals, emotions and logic did not work. When I bruised this persons ego centered around them doing something obviously stupid that was causing them physical pain they responded well. The person hurt their foot after we broke up and the doctor would not give them pain meds because they would not ask for fear of becoming addicted. They had however discussed their affinity for Mary Jane so I offered to buy them some pot and they refused. It's legal here but could not afford the trip to the special doctor or the pot itself. I swore fine and when you want your nose reattached for you seem to have your mind to remove it I will pay the plastic surgery. They asked what do you mean and I explained the concept of Cutting off the nose to spite the face. Then my help was accepted. So I would frame the argument around self betterment. Do not attempt to point out fallibility of the individual to self help. They love gifts. Maybe buy a book that deals with psychotherapy and includes something that resembles their problem. (Mean Mothers: Overcoming the Legacy of Hurt if they are female and maybe the lesser The Emotionally Absent Mother: A Guide to Self-Healing and Getting the Love You Missed
If male a lot of problems are so inherited from parents and learning about their parents flaws may help them self identify) A lot of important people in the world bare some of the dark triad traits and have learned through therapy how to be more successful and influence people.


Are there any online survey/questionnaire makers which allow use of sound clips? I am looking to create an online data collection tool which would involve questions where a short sound clip is played, and the respondents would need to use a rating scale (possibly a slider) to respond.

So far I've come across several sites which do not allow uploading sound clips - any recommendations?

Two such systems include Qualtrics and Inquisit. For example: https://www.qualtrics.com/support/survey-platform/survey-module/editing-questions/rich-content-editor/insert-media/


What are some books about the effect of childhood experiences on adult life? I would like to read some books about the effects of childhood experiences on the adult life. For an example, somewhere I read that adult males who had an aggressive father they are usually not aggressive (because they find it repulsive and inhumane), and also, they are not able to show anger in the proper dose when needed. The example may not be accurate but I hope I conveyed what I mean.
I have a PhD (not in neuroscience or psychology) so I think I can manage even a bit more academic oriented books. However, it would be nice to have some books suitable to average layman person too.
It would be nice someone could read such a book and by comparison to themselves realize that some trait of them is not actually normal and should be fixed.

This question is open to opinion, however, I cannot see how you can go wrong with buying the book Life-Span Human Development by Sigelman & Rider (now in its 8th edition) mentioned in @Chris' answer to What happens to someone missing teenage years of development?


Structural descriptions of neuronal networks are important for understanding brain dysfunctions; which dysfunctions, in particular? In a recent paper, we find this quote:

  The brain contains vast numbers of interconnected neurons that constitute anatomical and functional networks. Structural descriptions of neuronal network elements and connections make up the “connectome” of the brain (Hagmann, 2005; Sporns et al., 2005; Sporns, 2011), and are important for understanding normal brain function and disease-related dysfunction.

This quote is from the first paragraph in: T. B. Leergaard, C. C. Hilgetag and O. Sporns, Mapping the connectome: multi-level analysis of brain connectivity, Front. Neuroinform., 2012.

  Question: Understanding which dysfunctions, in particular, is aided by structural descriptions of neuronal networks?

Stam et al. have carried out a functional connectivity study in patients with Alzheimer's Disease. I don't know if that answers your question at all. Connectomics is just starting to kick off. It's far from certain that they it will end up being a key player in functional neuropathology in the coming decades, but it's one out of many promising new avenues of research.


Which animals are thought to possess some degree of a theory of mind? Most dog owners would insist that their dogs have a strong theory of mind, and I have read abstracts that support this idea - for instance, a dog who knows better than to snatch a piece of forbidden food from a plate on the floor while his or her master is looking becomes more likely to do so when the lights are turned off, which suggests that the dog understands that the owner can't see what he or she is doing in a dark room.  I've also noticed that a dog will react differently when he or she is intentionally hurt by a mischievous child than he or she does when someone accidentally steps on his or her tail or paw.  These phenomena suggest that dogs might understand that our perception is different from theirs, and that there is a difference between intentional harm and accidental harm.

Many of us would probably assume that higher primates are almost as skilled as we are in the use of the theory of mind, and again, I have seen research that seems to back this up.  A chimp is placed in a room with plexiglass walls.  The room faces a hallway.  A hole in the wall allows the chimp to grab fruit from a tray in the hallway.  A researcher walks into the hallway, picks up the tray, and throws it down the hall.  The chimp goes ballistic.  However, when the same process is repeated, but this time, the researcher pretends to accidentally trip over the tray, the chimp is less agitated, and instead of throwing a tantrum, he or she merely gestures towards the tray and waits to see if it will be returned to its original position.  This suggests that chimps know the difference between accidents and intentions, which is not particularly surprising, considering how complex (and dangerous) chimpanzee society is.

Add to this anecdotal reports of whales and dolphins apparently showing gratitude when humans assist them (removing nets in which they've become tangled, for instance), and many similar accounts.

Do we have any idea which nonhuman animals possess a theory of mind, at least to some degree?

Well, the areas most responsible for social cognition (or theory of mind) appear to be the right and left temporoparietal junctions, the right anterior superior temporal sulcus, the posterior cingulate, and the medial prefrontal cortex. [1][2] Of those, the right TPJ is perhaps the most important; for example, the response in the rTPJ shows a peak just at the time when someone’s thoughts are described. [3]

Given the perceived importance of the temporal lobe to theory of mind, it is probably a safe bet that you wouldn't find many non-mammals that experience ToM the way a human does.

Furthermore, among the many hypothesized 'signs' of ToM possession is the ability to recognize oneself in the mirror. This ability implies a level of self-awareness and identity awareness in the individual, and it appears that primates (chimpanzees and orangutans) are the only non-human animals that have successfully recognized themselves in the mirror. [4] Monkeys are also the only other animals to have confirmed rudimentary mirror neurons, which are hypothesized to play an important role in empathy and social cognition. However, there are pieces of evidence that suggest that mirror neuron networks may possibly exist in elephants, dogs, dolphins, and whales.

That being said, the evidence isn't wholly clear on this one, and is further augmented by the fact that we don't necessarily have a working cognitive model for ToM (outside of our verbal conceptual models, which are not exactly scientifically rigorous). Some researchers even believe that ToM is a uniquely human experience. However, until we can lock down what exactly it is we are looking for, this remains a tricky question to make any sort of scientifically rigorous assertion.

Sources used:

[1] Dodell-Feder, D., Koster-Hale, J., Bedny, M., Saxe, R. (2010). fMRI item analysis in a theory of mind task. NeuroImage.

[2] Deen, B., Koldewyn, K., Kanwisher, N., Saxe, R., (2015) Functional Organization of Social Perception and Cognition in the Superior Temporal Sulcus. Cerebral Cortex

[3] Young, L., Cushman, R., Hauser, M., & Saxe, R. (2007). The neural basis of the interaction between theory of mind and moral judgment. PNAS, 104(20), 8235-8240

[4] G.G. Gallup (1982). Self-awareness and the emergence of mind in primates.
Am. J. Primatol., pp. 237–248


What's the difference between computational neuroscience and systems neuroscience? I'm an engineer, interested in mental machinery, to imitate cognitive capabilities of the human mind into primitive artificial models. In this case, cognitive neuroscience (CogN) is something, apparently, relevant and important field.

But I have no clear idea about the differences between computational neuroscience (CompN) and systems neuroscience (SysN) and their relevance to my target. In my view, these two topics are very similar (if not the same!), because one need to analyze the brain and its systematic functionality by computational approaches. Furthermore, it is inevitable to consider system-driven perspective to be able to present computational interpretation for neural systems.

So, what is the subtle difference between SysN and CompN?
Which one should be taken into account within (in coordination with CogN) to studying of the mental functionality of the brain?

Thanks

EDIT: Someone else's answer to the first question, does which sound like a seminal viewpoint:

  I feel the question is ill-posed. Don’t pick a “field” to study. Pick
  a problem to study. Based on the problem selected one or another field
  may be more relevant for your work, but it is unlikely that any
  interesting question about cognition will fall wholly within the
  domain of any one classically defined area of neuroscience.

Systems neuroscience studies systems, such as the visual sensory system - from the light (input) to the cortical representation. Systems neuroscience generally implies an integrated approach that includes fundamental or basic neuroscience - the study of cellular and molecular functions of the nervous system(s) - and typically borders to behavioral or cognitive neuroscience.

Whereas cognitive neuroscience aims to explain the "biology of the mind" - for example, how is memory realized in the brain - systems neuroscience aims to explain how the brain works - for example, how does the brain give rise to vision.

Computational neuroscience is fundamentally a mathematical discipline that is realized using computers. It is used to both simulate (theoretical neuroscience) and validate in vivo and in vitro findings in silico. It includes the abstraction of general laws based (more or less) on empirical data. Generally, initial parameters are based on findings from basic neuroscience, which enables biophysically realistic models based on the functionality of neurons to be implemented. However, less realistic simplified models are often used to model neural networks that have an applied AI task. However, these models border to computer science and in particular AI and machine learning.

Neuroscience is a large field and there is a strong need to bridge the different disciplines that contribute to the science, not only through computational neuroscience, but also through neuroinformatics:

  The exponential growth of the data produced in neuroscience mean that
  computational approaches are fundamental to make sense of this information, including theoretical modelling and methods for large scale data analysis/integration that are capable  of handling and comparing data generated over such
  diverse timescales (e.g. synaptic versus  genetic  changes).  As  such,  quantitative  theoretical  neuroscience  must  be   gradually integrated with
  mainstream experimental neuroscience.
  —European Brain Council Consensus Statement - March 2016

In response to comment

"Basic neuroscience" requires an invasive study of neurons in order to study the molecular mechanisms of the cell - on the most basic level. That is why mostly animals are used in this type of study. (However, neuroanatomists also study human post-mortem brains, and molecular imaging can be used in humans, but on a different level of explanation - a whole-brain perspective - with less specificity of the causal mechanisms on the cellular level.) Molecular neuroscience studies, for example, the properties of different types of calcium channels. A famous computational model is the Hodgkin-Huxley model that is based on the study of aplysia. In this regard, basic neuroscience informs computational models that are bottom-up, but there are also top-down models that rely on pure psychology, and a range of models in-between.

N.B. I would be careful to use the term "exploratory", because this implies that the science proceeds without a hypothesis. That is rarely the case in the natural sciences, but some of the pioneering work is indeed exploratory.

I am a PhD student in Neuroscience working with humans. Some of my colleagues work with animals or cell cultures. One of my collaborators works in computational neuroscience and we are currently working on a new model together that we might be able to update based on the empirical findings in my lab. This type of collaboration is important, because the computational model "knows" more basic science, than I could possibly study in humans. That is why we can use computational models to test the limits of our findings - to test if our models of cognition are compatible with biophysical models, which are informed by principles derived from animal studies.


What can coma patients report about their experiences - if anything? Coma is correlated to a significant inactivity of the cerebral cortex and the reticular activating system, while other parts of the brain - e.g. the limbic system - might still show considerable activity.

My question is:

  Are there cases where people recovered from a coma and could later plausibly report experiences they made during the coma?

What kind of experiences would they typically report - if any? And how fine-grained can descriptions of such experiences be?

Examples:

"I felt that I were alive."
"I felt horrible/relaxed."
"I sometimes felt hungry."
"I felt that my mother was there."
"I somehow felt she touched me."
"I somehow heard her say my name."

Most surely, elaborate thoughts and complex emotions can not be recalled and plausibly reported (because they could not take place).

  What would such reports tell us about the neural basis of
  consciousness?

Are there forms of recoverable coma where the cerebral cortex and/or the reticular activating system is completely mute, i.e. without any measurable coordinated neural activity?

Do other parts of the brain necessarily show no measurable coordinated neural activity when the cerebral cortex and/or the reticular activating system doesn't?

The majority of people who recovered from coma did not report any experiences that occurred while they were in coma (clinically unresponsive, with absent or minimal brainstem reflexes, and with severely abnormal EEG). However, some people who had cardiac arrest or came very close to clinical death but were successfully revived reported later that they had conscious perceptual experiences during these critical periods, when they were in coma. This kind of experiences is called “near-death experience (NDE)” by Moody [1]. About 10% to 20% of such critical individuals reported near-death experiences (NDEs) [2]. NDEs include many experiences, such as seeing tunnel, light, and stars; out-of-body experiences; pleasant feelings; entering a door/gate, heaven, or hell; seeing deceased relatives, religious figures, or god; a life review; a conscious return into the body; etc. [2-5]

However, NDE is still an unsettled subject. Some believe that cumulated evidence so far shows that NDEs are real, that the mind and consciousness can exist without and outside the brain, and that the current understanding that the brain is the basis of consciousness and the mind is not correct [6-10].

Others believe that NDEs are neurophysiologic phenomena that occur while the brain is functioning in an abnormal state [5,11]. Evidence is that many mental phenomena that occur in NDEs can occur or be induced to occur in other non-coma, neurophysiologic states, such as sleep [4], meditation [12], simple partial seizures [13], certain drug-induced altered states of consciousness [11,14], and electrical stimulation and transcranial magnetic stimulation of the brain[15]. Interestingly, some investigators found that a surge of neurophysiological coherence and connectivity occurred within the first 30 sec after cardiac arrest and preceded isoelectric electroencephalogram in experimental rats [16]. Whether this also occurs in humans and is the basis of NDE occurrences or not needs further investigations.

The most crucial aspect of NDEs is whether the reported experiences occurred during coma/cardiac arrest or not. It is possible that those experiences occurred when the patients have recovered but were still in a confused or dream-like state and that the patients wrongly attributed the time of those experiences to when they were still in coma/had cardiac arrest; their reports were just sincere fallacy. However, this can be investigated in NDE experiencers who have out-of-body experiences and report seeing the scene and event when they are in coma/have cardiac arrest. If these NDE experiencers report (without the help from other people) the scene and events where and when they are in coma/have cardiac arrest correctly, it means their NDEs indeed occur during coma/cardiac arrest and, indeed, normal consciousness can exist without and outside a normally functioning brain – our understanding of the neural basis of consciousness has to be greatly revised from the root. AWARE [17] was the study that was designed to investigate this. Its results, however, were inconclusive. AWAREII [18] is a similar study that is expected to finish this year (2020). It is interesting to see how its results will come out.

So far, however, our present understanding of the neural basis of consciousness has been vindicated in clinical and experimental settings all around the world every day for a long time. It predicts that no conscious experiences, complex thoughts, or complex emotions can occur when one is in coma (clinically unresponsive, with absent or minimal brainstem reflexes, and with severely abnormal EEG), and no definite incidents of conscious experiences during coma have ever been reported.

References.

Moody, R. A. (1975). Life After Life. New York, NY: Bantam Press.
Kopel J. Near-death experiences in medicine. Proc (Bayl Univ Med Cent). 2019 Jan;32(1):163-164. doi: 10.1080/08998280.2018.1542478.
Belanti J, Perera M, Jagadheesan K. Phenomenology of near-death experiences: A cross-cultural perspective. Transcult Psychiatry. 2008 Mar;45(1):121-33. doi: 10.1177/1363461507088001.
Charland-Verville V, Jourdan JP, Thonnard M, Ledoux D, Donneau AF, Quertemont E, et al. Near-death experiences in non-life-threatening events and coma of different etiologies. Front Hum Neurosci. 2014;8:203. doi: 10.3389/fnhum.2014.00203.
Nelson K. Near-death experiences: Neuroscience perspectives on near-death experiences. Mo Med. 2015 Mar-Apr;112(2): 92-96.
Alexander E. Near-death experiences, The mind-body debate & the nature of reality. Mo Med. 2015 Jan-Feb;112(1):17-21.
Greyson B. Getting comfortable with near death experiences: An overview of near-death experiences. Mo Med. 2013 Nov-Dec;110(6):475-481.
Hagan JC III. Near-death experiences: I hope you are comfortable with them by now! Mo Med. 2015 Mar-Apr;112(2): 88-91.
Long J. Near-death experiences evidence for their reality. Mo Med. 2014 Sep-Oct;111(5):372-380.
van Lommel P. Near-death experiences: The experience of the self as real and not as an illusion. Ann N Y Acad Sci. 2011 Oct;1234:19-28. doi: 10.1111/j.1749-6632.2011.06080.x.
Martial C, Cassol H, Charland-Verville V, Pallavicini C, Sanz C, Zamberlan F, et al. Neurochemical models of near-death experiences: A large-scale study based on the semantic similarity of written reports. Conscious Cogn. 2019 Mar;69:52-69. doi: 10.1016/j.concog.2019.01.011.
Gordon WV, Shonin E, Dunn TJ, Sheffield D, Garcia-Campayo J, Griffiths MD. Meditation-induced near-death experiences: A 3-year longitudinal study. Mindfulness (N Y). 2018;9(6): 1794-1806. doi: 10.1007/s12671-018-0922-3.
Hoepner R, Labudda K, May TW, Schoendienst M, Woermann FG, Bien CG, et al. Ictal autoscopic phenomena and near death experiences: A study of five patients with ictal autoscopies. J Neurol. 2013 Mar;260(3):742-749. doi: 10.1007/s00415-012-6689-x.
Timmermann C, Roseman L, Williams L, Erritzoe D, Martial C, Cassol H, et al. DMT Models the Near-Death Experience. Front Psychol. 2018 Aug 15;9:1424. doi: 10.3389/fpsyg.2018.01424.
Blanke O, Thut G. Chapter 26. Inducing Out-of-body Experience. In: oup–Tall Tales about Mind and Brain (Typeset by SPi, Delhi). 2006 Jul 12.
Borjigin J, Lee U, Liu T, Pal D, Huff S, Klarr D, et al. Surge of neurophysiological coherence and connectivity in the dying brain. Proc Natl Acad Sci U S A. 2013 Aug 27;110(35):14432-7. doi: 10.1073/pnas.1308285110. /
Parnia S, Spearpoint K, de Vos G, Fenwick P, Goldberg D, Yang J, et al. AWARE - AWAreness during REsuscitation-a prospective study. Resuscitation. 2014 Dec;85(12):1799-1805. doi: http://dx.doi.org/10.1016/j.resuscitation.2014.09.004.
AWARE II. NHS Health Research Authority.


Does heritability define the person in terms of the population? I recently read a statement that goes like this: heritability is a population construct. Isn't heritability dependent on genetic differences? Can someone provide an example of what it means to be a population construct? Thanks

Heritability is the proportion of differences in some observable trait (the phenotype; e.g., intelligence, height, love for pizza) in a population that corresponds to differences in the genotype.

Heritability is estimated by comparing people who differ in terms of their genetic similarity and the non-genetic influences they are exposed to. For example, we know that monozygotic twins share 100% of their genes, whereas dizygotic twins share only 50% of their genes on average. If we compare twins that were raised in different homes (adopted twins) and monozygotic twins are more similar to each other than dizygotic twins we conclude that this difference overlaps with genetic differences, as expressed in a high heritability index.

Importantly, heritability does not describe the extent to which a person's individual characteristics were formed by genes or the environment, which is a frequent misconception. Heritability only describes the variance of a trait within a given population that corresponds to genetic differences in that population.

As described in Griffiths et al. (2000):

  It must be stressed that this measure of “genetic influence” tells us what part of the population’s variation in phenotype can be assigned to variation in genotype. It does not tell us what parts of an individual’s phenotype can be ascribed to its heredity and to its environment. This latter distinction is not a reasonable one. An individual’s phenotype is a consequence of the interaction between its genes and its sequence of environments. It clearly would be silly to say that you owe 60 inches of your height to genes and 10 inches to environment. All measures of the “importance” of genes are framed in terms of the proportion of variance ascribable to their variation.

How this restricts the interpretation of heritability becomes clearer if we imagine cases in which there is no genetic variation (everybody has the same gene) or there is no variation in the environment (everybody is raised in the same way). In the first case, every variation would correspond to environmental differences, in the second case every variation would correspond to genetic differences.

A nice example is described here:

  One example is hair color among Eskimos (N. Carlson & W Buskirt, 1997). The whole Eskimo population appears to have the same alleles for hair color, so for Eskimos, the heritability for hair color is 0.00, even though the color is under strong genetic control! It's 0.00 because there is no genetic variation for hair color.

Furthermore, it is important to point out that there can be considerable overlap between genes and environment. People with certain genes can search specific environments that others with different genes would not. These environments can then have a high impact on them. Nevertheless, because of the way in which heritability is defined, these environmental differences are ascribed to genetic differences. Furthermore, they depend on the possibility of seeking certain environments in a society. An example is described by Neisser and colleagues (1996):

  A high heritability does not mean that the environment has no impact on the development of a trait, or that learning is not involved. Vocabulary size, for example, is very substantially heritable (and highly correlated with
  general psychometric intelligence) although every word in an individual’s vocabulary is learned. In a society in which plenty of words are available in everyone’s environment-especially for individuals who are motivated
  to seek them out-the number of words that individuals actually learn depends to a considerable extent on their genetic predispositions.

For these reasons, heritability is a population construct, it hinges on the genetic and environmental variability within the population it describes.

References

Griffiths, A. J., et al. (2000). An Introduction to Genetic Analysis (7th ed.). New York: W. H. Freeman. http://www.ncbi.nlm.nih.gov/books/NBK21766/

Neisser, U., Boodoo, G., Bouchard Jr., T. J., Wade, A., Brody, N., Ceci, S. J., Halpern, D. F., et al. (1996). Intelligence: Knowns and unknowns. American Psychologist, 51, 77–101. doi:10.1037/0003-066X.51.2.77


Does straightening your back increase confidence? Background: I have always felt moderately socially insecure. Today I noticed that when I straighten my back from its normal crestfallen position, I feel a little more confident, and as if I were in attack mode.

Is there any relationship between straightening your back and confidence or other personal characteristics?

Brinol et al (2009)  suggest that your intuitions generalize.
From the abstract:

  Building on the notion of embodied attitudes, we examined how body
  postures can inﬂuence self-evaluations by affecting thought conﬁdence,
  a meta-cognitive process. Speciﬁcally, participants were asked to
  think about and write down their best or worse qualities while they
  were sitting down with their back erect and pushing their chest out
  (conﬁdent posture) or slouched forward with their back curved
  (doubtful posture). Then, participants completed a number of measures
  and reported their self-evaluations. In line with the self-validation
  hypothesis, we predicted and found that the effect of the direction of
  thoughts (positive/negative) on self-related attitudes was
  signiﬁcantly greater when participants wrote their thoughts in the
  conﬁdent than in the doubtful posture. These postures did not inﬂuence
  the number or quality of thoughts listed, but did have an impact on
  the conﬁdence with which people held their thoughts.

References

Briñol, P., Petty, R. E. & Wagner, B. (2009). Body posture effects on self-evaluation: A self-validation approach. European Journal of Social Psychology, 39, 6, 1053-1064. PDF


Why do people regret actions they didn't take when looking back on their lives? Is it true that individuals often regret recent actions (i.e., last few months) but when they look back on their lives, they tend to regret things that they have not done (or lack of actions) ?
If so, what causes this?

The classic reference for exactly what you are describing is Gilovich & Medvec, 1995 (LINK), the primary thesis of which is that "Actions, or errors of commission, generate more regret in the short term; but inactions, or errors of omission, produce more regret in the long run" (from the abstract). The authors explain that there are many factors that contribute to this general pattern; these factors are actually summarized quite nicely in their Table 3 below:

For a more complete description of these factors and a discussion of the relevant evidence, see the link I posted above to the Gilovich & Medvec paper.

References

Gilovich, T. & Medvec, V.H. (1995). The experience of regret: what, when, and why. Psychological review, 102, 379. PDF


What aspects of ACT-R are not contained within Spaun? ACT-R was the first big cognitive model and excels at modelling human behavioral data quite accurately.

Spaun, which is the world's largest functional brain model, took a lot of ACT-R's insights and applied them, most notably in it's model of the basal-ganglia-thalamus loop. More importantly, it did so in biologically plausible manner while ACT-R has been struggling recently to map it's functions onto brain areas and functionality.

That being said, ACT-R still seems to have an extremely active community and Spaun's developers are mostly restricted to the lab from which it originated. An obvious reason for not converting is if Spaun's range of cognitive functionality is missing some components of ACT-R.

What functionality of ACT-R isn't found in Spaun?

Both ACT-R and Spaun are modular, and could be extended to include capabilities of each other. Comparing the functionalities of the two architectures by a simple checklist is not the most appropriate way to compare them. Here are some points to consider:

1) ACT-R is primarily symbolic, whereas Spaun is a neural network. ACT-R is actually making a theoretical claim by committing to a symbolic architecture. This is one of the most famous debates in cognitive science; the upshot is that the two approaches each have limitations, and they go about solving problems in different ways. For a good starting point in this debate, see Fodor & Pylyshyn (1988).

2) Architecture aside, different algorithms can be implemented to solve the same problem. Maybe both Spaun and ACT-R can do simple declarative memory retrievals, but do they predict the same response times and accuracies for a given retrieval? I suspect they don't.

3) As mentioned in your answer, Spaun does not include a of long-term memory but does include working memory. In ACT-R, long-term memory and working memory are not distinct concepts; working memory can be construed as a subset of items in memory that are highly activated. There is no discrete distinction. This suggests that the structure of components in ACT-R is fundamentally different than Spaun.


What do you call sensations without stimuli? Sometimes, when you close your eyes in the dark, you see what looks like sparks or flashes. Sometimes when you are tired, your vision seems to shift sideways and realign, like someone bumped into a camera, although you didn't move your eyes. It seems to me that some of these apparent sensations are not caused by (external) stimuli to the sensory apparatus but rather by an "overexcited" nervous system.

Is there a term for such "mistakes" of the visual system? I don't know what terms to use to describe these phenomena in scientific reports.

Short answer
Visual hallucinations and, more specifically, phosphenes are the terms you are probably after.

Background
I'll basically provide a list of terminologies below, as your question seems to indicate you're walking on unfamiliar grounds with your research.

For a starters, sensations refer to the peripheral detection of stimuli. Perceptions are the higher cognitive, central correlate of those sensations involving the conscious awareness of them.
The sparks or flashes you're talking about may be caused peripherally (sensation level), but likely find their origins centrally (perceptual). This, because people with low-vision, or blind people lacking functional photoreceptors in their retinae can experience them too, and sometimes in exaggerated and pathological forms.
The visual field shifts are most likely caused by eye movements, unless you can provide solid sources to back up your thoughts that it can happen without eye movements. Likely, nystagmus or related involuntary eye movements are involved, which can be exaggerated by some physical conditions, again including blindness.
Now, as my knowledge is restricted to visual impairments, I can say that spontaneous spots of light are not sensations, but hallucinations. A hallucination being "...a sensory experience, possessing the compelling sense of reality of a true perception, but occurring without external stimulation of the relevant sensory organ. Specifically, they are elementary visual hallucinations, as opposed to complex visual hallucinations. An example of the latter is the Charles Bonnet Syndrome, where blind folks experience complex visual scenes, including faces.
Back to your question on elementary visual hallucinations, they are referred to as phosphenes, photopsiae, or unformed visual hallucinations, Typically they consist of colored or colorless bright lights, such as points, flashes, stars, and sparks. To provide some context to these terms: Phosphenes are generally used to describe benign phenomena, as well as for stimuli evoked by electrical stimulation of the retina or other visual centers (forget about the latter for the sake of simplicity, as these are not hallucinations anymore). Photospsias are generally used in the literature associated with retinal disease. Unformed hallucinations, personally, I've never encountered in my field of research, but the linked article below gives it as a last option, so I simply included it here too.

Reference
- Menen et al (2003), Survey of Ophthalmology; 48(1): 58–72


Manipulating the difficulty of guessing a correlation I am trying to generate correlations between random variables (two dimensional) with a defined linear relationship (in the $r$ sense), but with different visual patterns when plotted. I am trying to create a 'guess the correlation' task where I can systematically manipulate the difficulty for an observer to guess the linear relationship.

What I am doing now is given a correlation $r$ I generate the first and second values, $X_1$ and $X_2$, with $n$ samples from the standard normal distribution. Then from there I make $X_3$ a linear combination of the two $X_3 = r X_1 + \sqrt{1-r^2}\,X_2$

Then:  $Y_1 = \mu_1  + \sigma_1 X_1, \quad Y_2 = \mu_2 + \sigma_2 X_3$

And now $Y_1$ and $Y_2$ have a correlation $r$.

For manipulating the difficulty I've been playing with the parameters of the distribution and $n$, however, I am not satisfied with the results.

Any idea on how to systematically increase the difficulty of the task? (i.e., adding outliers, for instance etc).

Note: Difficulty is a cognitive/psychology question rather than a statistical one. I intend to test the notion of difficulty empirically (i.e., under a specific parameter combinations, people tend to do worse). The idea is to generate plots with varying parameters for a given correlation value (i.e., changing the number of points, the variance, outlier, functional form? etc). What are the parameters and what would be a systematic way to manipulate them.

You will probably need to do pilot testing to ascertain the difficulty of a given correlational task.

From pilot testing, you would need to quantify the difficulty of the task. One option would be the mean discrepancy between actual and predicted correlation. However, there would be other metrics of both degree of error and difficulty.

I would hypothesise that the easiest correlations to guess based on scatterplots would be strong linear relationships involving bivariate normal distributions and lots of data (e.g., n > 1000).

There are a whole bunch of things that you could try to make the task more difficult. Here's what comes to my mind:

Outliers (both outliers that increase the correlation and outliers that decrease the correlations); vary the number of outliers in a particular region; combine outliers that increase and decrease the correlation; make outliers even more extreme
Non-linear relationships (e.g., mixtures of linear and another function such as quadratic, cyclical, stepwise; power functions, logistic fucntions, circular, etc.)
bimodal distributions on one or both variables
Highly skewed distributions on one or both variables
Fewer data points
data that yield correlations only a little bit above or below zero
where there is a function like a quadratic, make the x depend on y rather than y depend on x.

More generally, I think that practice and feedback effects will also be relevant. I.e., it may be relevant to ascertain whether the differences in difficulty with novices also correspond to relative differences in difficulty with participants who have been exposed to the full range of items you have generated.


Informed Consent Research Question I am a member of a closed, fairly large private group on Facebook of former game show contestants.  Several years ago, another member posted a Google Forms version of the Asperger Quotient test, asking group members to take the test, to report their overall score (anonymous), and to answer a few demographic questions on the form.  After collecting about 300 responses, he shared the composite results with the group (who were enthusiastic about the idea).

I've since asked the member who composed the original post if he would be interested in turning this idea into a publishable research brief. I am a psychologist and faculty at a small university and could create the IRB/ submission at my institution.  My issue, though, involves about informed consent. The data is collected, but he did not include an informed consent statement with his Facebook post.  Should I scrap his data, create an informed consent, and then re-send out the AQ?  Or do you think I should submit a request to the IRB asking to use the existing data?
Thanks!

I'd recommend consulting informally with IRB staff at your institution beforehand, usually (and maybe especially at a smaller institution?) they are willing to help out a bit at the design stage. Once you find the right person to contact, I'd convey to them almost exactly what you've posted here (probably via email), plus a bit more background on the actual current form of the data.

IRBs can vary quite a bit on what they allow; there are minimum standards they are required to follow but I've seen IRBs go well beyond those standards at times. It may be that the IRB decides the data are anonymous enough and low risk enough that you don't even need consent; it may be that they won't allow it in any form unless you start from scratch (and contacting the people who originally participated may similarly not be allowed; you might be able to solicit the group but not the previous responders directly).

There is likely a blanket prohibition on you collecting data, then trying to go back and get consent to use it in another way, but your situation is a bit different in that you weren't the one collecting in the first place and the collection does not seem to meet the criteria for "research" at the time of collection.

These flow charts from HHS might help a bit if you are in the US. Following Chart 2 and then Chart 4/5, it is quite possible that this work could be exempt from full review (but at least at my institution, it is still the IRB that decides whether the exemption applies).


What is the name for the cognitive bias that ignores that extreme symptoms always tend to get less extreme? There are some long term diseases where the severity of your symptoms tend towards a 'normal'. So imagine plotting out the severity of the symptoms say, every day or every week, then drawing a line of best fit through them.

So over the long term, severity may change slowly. However in the short term, statistically speaking, it'll tend to be that if symptoms have been super bad for a short while, it'll tend to get better. And if symptoms have been very good for a short while, it'll tend to get worse.

There's a name for this trend. I'm not sure if it's actually a cognitive bias, it could be more of a statistical fallacy type thing. I can't remember the name... and I've searched for it in every way I can think of in google but no luck. I originally read about it in the context of pseudoscience treatments. So someone has a long term condition, they have a very 'bad year', they go see say... a homeopath, and then they get a bit better and they ascribe their improvement to the homeopathy where as in fact, statistically speaking they were likely to have gotten a bit better on their own.

The statistical phenomenon you are referring to is called regression to the mean. It describes the fact that extreme measurements which are affected by random fluctuation will tend to be closer to the average in subsequent measurements. This phenomenon is not limited to clinical symptoms but occurs for any measurement that is selected for its extremity.

As an example, you let students take two tests that are designed to assess the same underlying aptitude. Then you look at the 5% best and the 5% worst performers in the first test. In the second test, the score of the high performing students will likely drop to some extent and the score of the low performing students will likely rise to some extent, even though the aptitude has not changed. This is because the test results are affected by random variation (they are not perfectly correlated) that is independent from the aptitude.

The failure to take statistical regression into account gives rise to the so-called regression fallacy. The regression fallacy refers to the tendency to attribute the change of extreme scores to spurious causal reasons. As a frequent example, if a football team loses some games and fires the coach, subsequent increases in performance may be explained with this fact even though it was just due to chance.


Link between visual-spatial + verbal working memory and intelligence/academic achievement? What is the link between someone's visual and spatial working memory, their verbal working memory, and different types of cognitive abilities or tasks? More specifically, intelligence tests (WAIS, Stanford Binet, etc.) and would this relate to educational outcomes in different fields (maybe SAT scores, graduation rates in different fields, and GPA, etc.)? Is there a relationship between these variables? Some cite working memory as the most important predictor of early academic success.

Somebody who has a strong verbal working memory may generally perform well on other types of verbal tasks included on intelligence tests: vocabulary, verbal reasoning, analogies, antynoms, etc. And be better suited to learn about fields such as literature, biology, foreign languages, etc. because there is a lot of linguistic mastery required in these disciplines.

Or on the other hand, if somebody has a strong visual-spatial working memory they may generally perform well on intelligence tests on other types of visual-spatial tasks that also recruit reasoning ability and long-term memory. And would be better suited to learning about fields such as physics, mathematics, art, architecture, etc. because there is more of a visual-spatial component in these disciplines.

Of course, there are many other factors that affect ability and learning. Working memory would be a small determinant but a determinant nonetheless. Furthermore, there is research which shows a link between spatial ability and achievement in STEM subjects up to graduate level studies for example.

Cognitive abilities from both of these broad areas (overall visual-spatial and verbal ability) certainly overlap highly — same with other types of reasoning abilities such as numerical and logical. However, I assume each area has a bias as to what types of cognitive abilities are used more.

There seems to be a very strong correlation between the two types of working memory or short-term memory. That's what I wanted to find out mainly: What is the relationship between the different types of working memory or short-term memory and other types of reasoning abilities (non-working memory reasoning tasks including verbal ability, numerical, spatial, etc.)? Are the different measures of short-term and working memory measuring approximately the same thing?

How common is the occurance of individuals that have poor verbal working memory and high verbal reasoning scores on intelligence tests for example? How about for visual-spatial working memory and non-working memory visual-spatial scores on intelligence tests?

I've read a few papers on this subject but am unsure of the answer.

Hopefully, someone can point me in the right direction. Thanks.

References:

Timothy F. Brady, Talia Konkle, George A. Alvarez; A review of visual memory capacity: Beyond individual items and toward structured representations. Journal of Vision 2011;11(5):4. doi: 10.1167/11.5.4.

Teixeira, Rosani Aparecida Antunes, Zachi, Elaine Cristina, Roque, Daniela Tsubota, Taub, Anita, & Ventura, Dora Fix. (2011). Memory span measured by the spatial span tests of the Cambridge Neuropsychological Test Automated Battery in a group of Brazilian children and adolescents. Dementia & Neuropsychologia, 5(2), 129-134. https://dx.doi.org/10.1590/S1980-57642011DN05020012

Spatial Ability: A Neglected Talent in Educational and Occupational Settings
Harrison J. Kell & David Lubinski
Roeper Review Vol. 35 , Iss. 4,2013

Work in progress -

  What is the relationship between the different types of working memory or short-term memory and other types of reasoning abilities (non-working memory reasoning tasks including verbal ability, numerical, spatial, etc.)? Are the different measures of short-term and working memory measuring approximately the same thing?

This is  a good question, but you are a funny person: say hello to positive manifold.

The concept of the general factor of intelligence emerges from the observation that all cognitive tasks are positive correlated with one another, or display positive manifold. It's as though they're all tapping into this invisible phlogiston, the general factor of intelligence/psychometric g. Perhaps the following puts it more succinctly:

From: Sternberg, R. J., & Kaufman, S. B. (Eds.). (2011). The Cambridge handbook of intelligence. Cambridge University Press.

  Is there a relationship between these variables?

As above. The reason why WM is most predictive of academic achievement is essentially because it's thought that it's tapping into the general factor most.

  Somebody who has a strong verbal working memory may generally… Or on the other hand, if somebody has a strong visual-spatial working memory they may generally perform well on intelligence tests on other types of visual-spatial tasks

What you are saying sounds perfectly cogent, but you are making one important assumption here that I don't necessarily agree with: that visuo-spatial WM and verbal WM are so thoroughly dissociable that one can have one that is stronger than the other in the way that I kick a ball real good with my right foot, but am a total ponce with my left foot. Although they are considered separate cognitive structures, I would anticipate that they're still very highly correlated in most people, individual differences notwithstanding.

Here is a snippet I have found:

However, later in the same reference, there is an interesting chapter on individual differences in visuo-spatial WM ability. In it, the authors describe a sample comprising children with learning disabilities where the deficit could be characterised as High Verbal/Low Visuo-Spatial intelligence, and vice-versa. Under some circumstances, the abilities can be dissociated:

From: Cornoldi, C., & Vecchi, T. (2004). Visuo-spatial working memory and individual differences. Psychology Press.

  Of course, there are many other factors that affect ability and learning. Working memory would be a small determinant but a determinant nonetheless.

Here, I disagree. Have you ever attempted to entertain a complicated concept comprising multiple components, only to have it "fall out of your mind" for lack of a better word? In order to process complicated concepts, you need to have some. Working memory is king, and all other abilities are subservient to it.

  How common is the occurance of individuals that have poor verbal working memory and high verbal reasoning scores on intelligence tests for example?

I am going to make a bold a priori claim: it is simply not possible for this to occur.

To argue my point, consider what you are implying: suppose someone was reading a passage of text with a long sentence. If they had very low verbal WMC, what would happen is that the beginning of the sentence would decay before they got to the end; they could never hold the information in the fore of the mind sufficiently long enough to process it, prod it, and synthesise an idea. Likewise for a sophisticated verbal reasoning task; a complex reasoning item has multiple components that must be considered simultaneously.

This reference describes it perfectly:

From: Cowan, N. (2012). Working memory capacity. Psychology press.

Effectively, what I am saying is that robust WMC is a necessary but insufficient component of verbal reasoning ability.

  How about for visual-spatial working memory and non-working memory visual-spatial scores on intelligence tests?

I'm a little confused by this, but I think you're making the same analogy as above. Same deal. However, I will make the point that WMC would represent the bottleneck in cognitive resources that would predict performance.

Having made this claim simply from first principles, let me dig up some evidence for my claims.


What's the psychological issue name of fear of people? With the issue of being afraid of doing anything before people, one has to work hard on self control to prevent the body shaking on every tiny action, like hold a pen, drink water, etc, and when there's many people looking at him/her, it becomes almost impossible to hold shaking, to speak normally, or to think. This person is subconsciously in fear of people unhappy(?) with his actions, even though he knows there's nothing wrong with his behavior.

Is this a typical case in Psychology? Is there a name for it?

Scenario for some background information his mother died when he was very young, his father don't like him, never talked to him except call everyone dinner, never smiled to him, never spent time with him, never gave any recognition even he got full marks, curse and beat him on whatever excuse when not in good mood.

He lived in a room with a big window in the wall next to the living room(a request for curtain was rejected), he had no idea why father dissatisfied with him (he's always one of the best in his class during student period and never asked for anything from his father, if exclude care), but been used to keep an ear out on his father all the time when at home, for whenever his father step into the living room where he would be seen through the window, he could sit as straight as he can before his desk and try not to move a bit, he didn't want to give him any excuse to curse, to beat.

The general symptoms (NOT the background scenario) may point to a psychological disorter called  social phobia :

Social anxiety disorder (SAD), also known as social phobia, is an
anxiety disorder characterized by a significant amount of fear in one
or more social situations, causing considerable distress and impaired
ability to function in at least some parts of daily life.
...
Physical symptoms often include excessive blushing, excess sweating, trembling, palpitations, and nausea. Stammering may be present, along with rapid speech.
...
The first line treatment for social anxiety disorder is cognitive
behavioral therapy (CBT) ... . The cognitive and behavioral components
seek  to change thought patterns and physical reactions to
anxiety-inducing
situations. ... . Prescribed medications include several
classes of antidepressants: selective serotonin reuptake inhibitors
(SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and
monoamine oxidase inhibitors (MAOIs)
...
It is the most common anxiety disorder with up to 10% of people being affected at some point in their life


In NEURON simulator, what is the command for "Init & Run" button? Sometimes other windows obscure the UI, and I would like to type in the command from the NEURON console.

Typing the following into the NEURON console will reset and run the simulation:

  run()


How much sleep is needed for peak cognitive performance? How much sleep is needed for peak cognitive performance? If some were to, for example, wake up one morning at 12:30PM, would a sleeping pill help obtain better sleep required for that performance the next morning at 08:00AM? And when would the optimal time be for the consumption of that sleeping pill? Is the amount of drawbacks in cognitive performance perceptible for 4.5 hours of sleep vs. 7 hours of sleep?

How much sleep is needed for peak cognitive performance. If some were for >example wake up one morning at 12:30 pm would a sleeping pill help obtain >better sleep required for that performance the next morning at 08:00 am ?

It depends on what pharmacotherapies - per the clinical judgement of their treating physician - one may have consumed. Conceptually, we might consider the two most psychopharmacologically relevant agents to be psychostimulants (coll. "uppers") and sedatives (coll. "downers" aka "goofballs").

Regarding sedatives, one's biggest concern would be a residual hangover effect. This is influenced by the agent's half-life (t½). For future reference, some 8 drug half-lives are needed for complete elimination. A short-acting benzodiazepine such as midazolam (t½ = several hours) is less likely to have residual effects than a long-acting barbiturate such as phenobarbital (t½ = 100+ hours). Non-benzodiazepine sedatives such as zolpidem appear so-so with regards to hangover, zaleplon seems to fair considerably better [1]. sedating antihistamines are horrendous [2]. If one had an enterically-coated "XR" tablet, one might do well to crush it up before swallowing, to ensure a more amenable pharmacokinetic profile.

  Is it perceptable the amount of drawbacks in cognitive performance in
  a situation of 4.5 hrs of sleep vs 7 hrs of sleep?

First, a caveat: individual differences apply here [3]. You know the answer for your own cognitive faculties better than anyone else. Interestingly, here is one paper that shows relatively modest drops in performance after acute sleep deprivation; chronic sleep deprivation, however, appears to have a deleterious dose-dependent effect [4].

Of direct relevance to your actual question, the above study notes:

Based on these findings, it appears that the inflection point (i.e. the minimum amount of nightly sleep required to achieve a state of equilibrium in which daytime alertness and performance can be maintained at a stable, albeit reduced, level) is approximately 4 h per night. [4]

Who'd've thunk, right?

The issue boils down to this:

Will the time you spend attempting to encode new memories into your LTM be more beneficial than the loss in attentional and executive function, as well as loss of potential REM-related memory consolidation and subsequent recall at the time of your examination?

When it comes to one's own therapeutic needs, it is always prudent that one consult with their treating physician. Here are my own reckless thoughts on the matter:

Ideal situation: if one's healthcare practitioner has prescribed them the sedative sodium oxybate (better known as GHB), then per oral administration of 4-5 grams GHB, followed by rapid onset of 4 hours of deep, refreshing sleep, might be indicated [5]. It would appear very unfortunate that GHB developed a reputation as a date rape drug, as anecdotally, some individuals consider it the "perfect sleep aid", particularly during exam periods.
If one's healthcare practitioner has prescribed them any of the following psychostimulants: d-amphetamine [6], modafinil [6] or perhaps methylphenidate they may wish to consider - per the recommendation of their physician, of course - skipping sleep entirely. Obviously, this is contingent upon their ability to recover following completion  of their work, study or family-related responsibilities, but may result in greater performance relative to brief, fragmented sleep.
If one's healthcare practitioner has prescribed them a short-acting benzodiazepine, one may still find that their sleep disorder is refractory and follows this particular clinical course: sleep from 10 pm  to 2-4 am, awakening, titration of caffeine as indicated. They may find that 4-6 hours post-awakening, their cognitive abilities are better than had they slept the same amount of time and awoken closer to 8 am.[7]

Remain valiant, soldier. Some people's best exam performances have come from around 3-4 hours of broken sleep care of a third of a bottle of Jack Daniels.

References

[1] A comparison of the residual effects of zaleplon and zolpidem following administration 5 to 2 h before awakening http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2125.1999.00024.x/epdf

[2] Next-Day Residual Sedative Effect After Nighttime Administration of an Over-the-Counter Antihistamine Sleep Aid, Diphenhydramine, Measured by Positron Emission Tomography http://journals.lww.com/psychopharmacology/Abstract/2010/12000/Next_Day_Residual_Sedative_Effect_After_Nighttime.9.aspx

[3] Inter- and intra-individual variability in performance near the circadian nadir during sleep deprivation. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2869.2004.00429.x/full

[4] Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose-response study.
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2869.2003.00337.x/epdf

[5] Enhancing Slow Wave Sleep with Sodium Oxybate Reduces the Behavioral and
Physiological Impact of Sleep Loss.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938863/pdf/aasm.33.9.1217.pdf

[6] Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. I. Effects on mood, fatigue, cognitive performance and body temperature. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2869.1995.tb00172.x/abstract

[7] Personal communications with myself.


What is the neurological mechanism behind the "fear of failure"? Sometimes, the fear of failing at something can be debilitating, and more often than not present a barrier for that person to even try new things - the locus of the fear can be quite different between people - ranging from academic, sporting and relationships and a whole lot more.

So, my question is, what is the neurological mechanism that results in the fear of failure?

According neurological perspective,  Amygdala  is involved in pleasurable emotional learning as well as fearful emotional learning. awareness of the aversive nature of  stimuli is sufficient to guide our actions. We avoid dangerous neighborhoods
or shark-infested waters, not mainly because we have been
 attacked by sharks in those locations, but instead
because we might have been given information regarding the stimulus aversive characteristics.
Previous research did substantiate on basis of humans using fear conditioning. they had had found that the amygdala is not completely important in terms learning or developing of an external, cognitive representation of the aversive characters of a stimulus or event .
This cognitive representation that depends on the hippocampal memory
system, which is significant in terms of developing declarative memories, which leads to recalling of past failed experience from hippocampus and feeling sense of fear of failure in future outcomes .although, the amygdala is important for expressing conditioned fear response towards the  same stimuli.
refrence : Phelps, E., O'Connor, K., Gatenby, J., Gore, J., Grillon, C., & Davis, M. (2001). Activation of the left amygdala to a cognitive representation of fear. Nature Neuroscience, 4(4), 437-441. doi: 10.1038/86110


Why does a neuron choose to connect to another? I have been reading about neuron creation, guidance cues and all sorts of highly complex mechanisms used to allow one neuron axon to extend or connect - but to what end?

Why does one neuron end up connecting to another? (instead of all the others)

Donald Hebb originally formulated what would later come to be known as spike-time dependent plasticity by famously stating "neurons that fire together wire together". In actuality, the firing has to be sequential (not simultaneous) and causal: if a neuron A fires and causes B to consequently fire, the synaptic strength between them increases. This is how the brain implements learning and memory. [1] This principle fits with the idea that the brain essentially learns causal relationships that exist in the world, as formalized in the Bayesian brain hypothesis [2].

[1] Markram et al., "A history of spike-timing-dependent plasticity": http://infoscience.epfl.ch/record/168812/files/fnsyn-03-00004.pdf

[2] Clark et al., "Whatever next? Predictive brains, situated agents, and the future of cognitive science": http://www.fil.ion.ucl.ac.uk/~karl/Whatever%20next.pdf


What is the location of the center-surround receptive fields of retinal ganglion cells? I have read wikipedia article about receptive fields of visual system and it states the following:

  The receptive field is often identified as the region of the retina where the action of light alters the firing of the neuron. In retinal ganglion cells (see below), this area of the retina would encompass all the photoreceptors, all the rods and cones from one eye.

I understand the part where it says that the neurons firing increases as we put light on the center of the receptive (for the ON center type) and etc.

What I'm not sure about is the location of this circle, in other words, where is this circle that we put light on?

What I think is that the circle is the area of retina where we have the rod and cone shaped photoreceptors. Does this means that for every ganglion cell the photoreceptors connected to it are always shaped like a circle ?

A nice illustrative image of how the photoreceptors connect to the retinal ganglion cell (RGC), and thereby facilitate the center-surround structure is provided in figure 1 below. It shows a cross section through the retina.

Fig. 1. Photoreceptor organization and connections to the retinal ganglion cell. source: McGill University

The receptive fields (RFs) are determined by the number of photoreceptors connected to the RFs. RFs are smaller in the central high acuity area of the retina (the fovea) and increase in size more eccentrically. As a result, visual acuity is highest in the center visual field, and degrades more eccentrically in the field of view.