How do neurons decide how to alter their output signals? In computer science, neural networks are trained using backpropagation and other methods. Backpropagation heavily relies on mathematical formulas to describe how the weights should be changed throughout the network to effect the final output of the system. Biological neurons need to be able to adjust as well, if I'm not mistaken. What happens within a neuron to cause it to adjust its output? In other words, are biological neurons "trained" and if so, what is the process behind it?

This will be a long post. FYI.

To my knowledge, there is no evidence for back propagation in the brain. If you're interested specifically in that topic, Geoffrey Hinton (Dept. of CS @ UofT) has written about it. I'll try to focus on the biology.

Some basic neurophysiology first. Neurons have a slightly negative electrical resting potential (prototypically ~-70 mV). When they fire (following depolarization) this increases. As you may guess, they can also hyperpolarize (less potential to fire an impulse). As you may also be able to guess, other neurons in the network can influence one another to make them more or less likely to fire. This, and indeed most, neuron-neuron communication occurs at synapses. A synapse is a small gap between the presynaptic neuron and postsynaptic neuron, as you're likely already aware. Respectively, these correspond to an axon (sending a signal) and a dendrite (receiving a signal). Long story short, when depolarized the presynaptic neuron releases neurotransmitters (NT) which are received by the post synaptic neuron. This results in changes in concentration of ions in the postsynaptic neuron (inside vs. outside of the neuron). This can result in the postsynaptic neuron firing itself. The  ions primarily implicated in this are Sodium (Na+) and Potassium (K+), transduced though ion specific Na+ and K+ ion channels in neuronal membranes.

One of the most critical ions related to your question, however, is Calcium (specifically, Ca2+). This ion often acts as an intracellular messenger, that is when it is 'let into' the cell after that neuron receives an impulse, it activates biochemical processes inside the neuron, e.g., to produce more of a protein.

How neurons actually learn has been a difficult problem to model. We know that neurons can potentate, that is a neuron can come to exert more control over the firing of another neuron. Indeed, it has been known for a long time that firing neurons strengthen connections. The famous aphorism for this is "neurons that fire together, wire together" (coined by the brilliant scientist Carla Shatz, now at Stanford). The problem is that if neurons just kept getting stronger, it leaves no room for information to be 'unlearned', which it is obvious it can be, for new information to be added to the system, or, indeed, information to ever be really learned at all. You'll see why in a moment.

One attempt to model the problem of neuronal learning is Beinenstock Cooper and Munro (BCM) Theory. Its basic proposition is that a connection that was once weak can become strong (and vica versa).
Specifically, what it attempts to model can be thought of as follows:

Imagine we have three stimuli (e.g., red, green, blue) and three cells. Before much exposure, all of these neurons respond ~equally to each of the stimuli (colors). After exposure the neurons respond differentially, that is neuron 1 might respond strongest to red; neuron 2 to green; and neuron 3 to blue. We might call this 'learning' because we wittness an increase in responding to a stimuli but also -- and this is critical -- a decrease in responding to other stimuli.

Biologically, one heavily implicated mechanism in this process is the N-methyl-D-aspartate receptor (NMDAR). Following binding of glutamate (a NT), this receptor allows Ca2+ into the postsynaptic cell. This animates intracellular events that result in either potentiation (typically in the form of Long Term Potnetation [LTP]) or depression (typically in the form of Long Term Depression [LTD]). In short, an increase or decrease a presynaptic neurons' ability to exert control over the postsynaptic neuron.

In simple terms:

> When low amounts of Ca2+ are conducted through the NMDAR --> LTD
> When hight amounts of Ca2+ are conducted through the NMDAR --> LTP

Critically, there is a modification threshold. This is the point at which LTD turns into LTP. This is represented by the greek letter theta (θ). BCM theory proposes a shifting threshold. If a synapse gets very strong, then θ shifts such that it becomes difficult to strengthen the connection further and easier to weaken it. Likewise, if a synapse becomes very depressed, θ will shift to allow it to more easily become potentiated and harder to weaken it.

For example, graphically you can visualize potentiation as the threshold shifting to the right. That is, the amount of Ca2+ that would have produced potentiation, now produces depression. The reverse, obviously, can also happen.

As you can see, what we've arrived at is something that looks rather computational. While I am not aware of a truly precise mathematical description of this process, it is obvious that such a description is, in principle, possible. You can see the math. proposed currently here (it seems implausible it could be that simple to me...and the assumptions made seem daft, but that's just my own commentary).
There are precise models of neuronal potentials and people are trying to put BCM (or something like it) into very precise terms. As you can image, this is extremely difficult because of the complexity of the biology, especially what Ca2+ is actually doing in the cell. In many ways, that is still a black box although we're learning about it at a very rapid rate.

In closing, biology seems to have solved the problem of learning very differently than computer scientists. As someone with both a mathematics and neuroscience background, I find the fact that this is possible to be simply incredible.


How to restore and maintain a healthy sleep pattern? Background: Some people over holiday periods or weekends get into sleep patterns that involve waking up very late in the day (e.g., 1pm), and then going to bed quite late (e.g.,, 4am). Such people can find it very difficult to bring back their sleep pattern to be in line with more regular day time rhythms (i.e., waking up between 6am and 10am). When earlier wake-up is attempted, this can result in feelings of fatigue and low mood.  Such attempts can even fail, when the person sleeps through the alarm clock.

General questions:

How can a sleep pattern be effectively re-aligned with normal day time rhythms?
What are effective strategies for maintaining a regular sleep pattern?
Is there any specific research on what strategies work best?

Yang et al. (2001) study this exact question. They administered 6 mg of melatonin on Sunday afternoon to subjects that had delayed sleep-wake schedules for the two prior days. They found that

  On Sunday, melatonin administration increased the sleepiness throughout the evening and reduced sleep onset latency at bedtime. On Monday morning, subjective sleepiness was decreased in the melatonin condition.

Kolla & Auger (2011) deal with resetting the internal clock for jetlag and night shift workers. Even though the situation is not identical, I think their main recommendations for adjusting the internal clock are relevant:

  Exposure to bright light in the hours leading up to the patient’s minimum core body temperature tends to push the internal clock later in time, whereas bright light in the hours immediately afterward pushes the clock earlier in time.

(minimum core body temperature is usually 2-3 hours before wakeup time).
So in other words, in order to re-align from wakeup at 1pm to 6-10am one should wake up as early as possible, and go out to be exposed to sunlight (or use an artificial light source).

They also discuss the use of drugs such as melatonin and caffeine.

References

Yang, C. M., Spielman, A. J., D Ambrosio, P., Serizawa, S., Nunes, J., & Birnbaum, J. (2001). A single dose of melatonin prevents the phase delay associated with a delayed weekend sleep pattern. Sleep, 24(3), 272-281. Full text PDF
Kolla, B. P., & Auger, R. R. (2011). Jet lag and shift work sleep disorders: How to help reset the internal clock. Cleveland Clinic Journal of Medicine, 78(10), 675-684. Full text.


Do bullies pick on sociopaths? As a percentage of their endeavours, do those with a tendency to use bullying focus more or less on sociopaths as a per capita of their targets?

As a percentage of their endeavours, do those with a tendency to use
  bullying focus more or less on sociopaths as a per capita of their
  targets?

Thanks for this interesting question. Based on my research the short answer appears to be that there is no clear evidence either way. The longer answer is that this is probably too complicated a question to easily answer.

Explanation

Based on psychology today I take sociopaths to be those who have:

A disregard for laws and social mores
A disregard for the rights of others
A failure to feel remorse or guilt
A tendency to display violent behavior

It is also important to consider that sociopaths develop these traits rather than being born with them, like psychopaths are (see quote from psychology today 1).

  Psychopathy is related to a physiological defect that results in the
  underdevelopment of the part of the brain responsible for impulse
  control and emotions. Sociopathy, on the other hand, is more likely
  the product of childhood trauma and physical/emotional abuse. Because
  sociopathy appears to be learned rather than innate, sociopaths are
  capable of empathy in certain limited circumstances but not in others,
  and with a few individuals but not others.

The literature on child bullying suggests that both bullies and victims tend to be more likely to have psychiatric disorders, such as sociopathy. The rates are 13% for bullies/ 8% for victims {1}. This suggests that 92% of those who are bullied are not sociopaths, but it fails to control for the fact that fewer individuals have sociopathic tendencies at that age. What is really needed is a test comparing two samples of children, on with sociopathic tendencies and one without.

An additional complication with this question is that it may be the case that children become sociopaths due to being bullied rather than being bullied because they are sociopaths {2,3}

Indeed some research {e.g., 2} suggests that anti-social personality disorder (which includes sociopathy) is the most common disorder amongst victims of bullying.

I hope this answer has been useful. Please let me know if you would like more information or need clarification on any points.

References:

{1} Copeland, W. E., et al. (2013). "Adult psychiatric outcomes of bullying and being bullied by peers in childhood and adolescence." JAMA psychiatry 70(4): 419-426.

{2} Sourander, A., et al. (2007). "What is the early adulthood outcome of boys who bully or are bullied in childhood? The Finnish “From a Boy to a Man” study." Pediatrics 120(2): 397-404.

{3} Arseneault, L., et al. (2010). "Bullying victimization in youths and mental health problems:‘Much ado about nothing’?" Psychological Medicine 40(05): 717-729.


What is the term for judging based on a simulation of the same parameters on oneself Allow me to outline the observed process and three hypothetical examples below. For the sake of keeping the samples simple, I will ignore prior moral or religious convictions that a regular person would hold.
A person is confronted with an issue or approach to be judged. The person places themselves in the hypothetical situation and evaluates the implications for themselves according to their beliefs and convictions. The outcome of the evaluation determine the person's stance on the issue.
What is the term for this decision mechanism?
I figured "empathy" at first but that would require emotional transference with a real or hypothetical individual which is not given in this case. "Reverse Projection" came to mind as well, but it is a very loose fit and projection usually implies the unawareness of the person projecting while the process above is not influenced by the person's awareness.

Examples of mechanism in use:
Issue: Is killing good or bad?
Person:
If someone were to kill me, it would end my life which is bad. --> Killing is bad.
Issue: Should a government provide free healthcare financed by taxation to everyone without restriction?
Person A (history of health issues, low income job, insecure):
If I become sick again, I may not be able to afford the treatment myself. The added taxation will not concern my income bracket. The added security net thus increases chances of my survival at no or little expense to me. --> Yes, a government should provide free healthcare financed by taxation to everyone without restriction.
Person B (health freak, high income job, arrogant):
I take care of my health which is why I am not sick. The added taxation would take away from the money I make while providing no additional benefit to me. --> No, a government should not provide free healthcare financed by taxation to everyone without restriction.

In naïve realism, the subject acknowledges others' points of view while affirming the superiority of his/her own. Ross and Ward (1996) review the literature. I tried to write a summary of their fine paper, but I couldn't do it justice. I provide a link to it below.

In selfishness or unenlightened self-interest, the subject may consider multiple points of view, but ultimately chooses by myopically predicting maximal net personal gain.

In philosophy, moral relativism is concerned with (inter-personal or inter-group) differences in moral judgements, and whether and how they can be reconciled. My point here is that your subjects' moral relativistic beliefs may impact their decision mechanisms and thus may be worth surveying.

References

  Ross, L., & Ward, A. (1996) Naive realism in everyday life: Implications for social conflict and misunderstanding. In T. Brown, E. S. Reed & E. Turiel (Eds.), Values and knowledge (pp. 103–135). Hillsdale, NJ: Erlbaum. [pdf]


Is it possible that listening same music with your partner can synchronize emotionally? Music forces us to feel emotions. Some music calms us, some music give us energy. What emotions music makes us feel can be different in each person but generally gives same emotions to us.

We have emotional turbulence in our daily routine. Sometimes our emotions sync with our partner but sometimes not. Is it possible that listening the same music with your partner can synchronize emotionally? Is there any scientific research for that? My field is not psychology so I am asking to you.

I think that one of the most basic and universal responses a person can have to music is engagement. When listeners are engaged with music, they follow the sounds closely connecting in an affective way to what they hear.
Moreover, music listening and music therapy is becoming an important topic of social neuroscience scientific inquiry (Kamioka et al., 2014).
This branch of research is facilitated by Hyperscanning EEG which provides the opportunity to explore dynamic brain activities between two or more participants (Liu et al., 2018).
I'd like to suggest to you the following study by Lindenberger and colleagues (2009).
The authors recorded EEG from the brains of pairs of guitarists playing a short melody together to investigate the rate of cortical synchronization in the course of music-driven actions.
In order to measure the rate of brain synchronization, they implemented the phase-locking index (PLI) which reflects invariants of phases across trials measured from single electrodes. As you can see in the first figure both the participants playing and listening to each other music showed fronto-central activity and Synchronization measured by the PLI index suggested that the activity is the highest at fronto-central sites. Especially, in the image below you can see the PLI distribution in the fronto-central brain regions at the theta frequency.

Finally, they used another index called Interbrain Phase Coherence (IPC) which represents the degree of constancy in phase differences across trial between two electrodes measuring the activity from two different brains.
In the figure below you can see synchronization between brains as measured by IPC: coherence was also strongest for fronto-central connections.

I hope that this paper partly answered your doubts. I do not know any study directly investigating brain synchronization in romantic couples, but if you think that romantic couples can be a discriminating factor to study brain synchronization while listening or practising music you could put on an experiment that considers romantic couples as an experimental group and friends/acquaintances as a control group.
Always remember, however, that you must justify the choice of your experimental groups with strong literature.
REFERENCES

Kamioka H, Tsutani K, Yamada M, Park H, Okuizumi H, Tsuruoka K, Honda T, Okada S, Park S. (2014)Effectiveness of music therapy: a summary of systematic reviews based on randomized controlled trials of music interventions. DOVEPRESS. http://dx.doi.org/10.2147/PPA.S61340
Difei Liu, Shen Liu, Xiaoming Liu, Chong Zhang, Aosika Li, Chenggong Jin, Yijun Chen, Hangwei Wang and Xiaochu Zhang. Interactive Brain Activity: Review and Progress on EEG-Based Hyperscanning in Social Interactions. Front. Psychol., 08 October 2018 | https://doi.org/10.3389/fpsyg.2018.01862
Ulman Lindenberger, Shu-Chen Li, Walter Gruber and Viktor Müller. Brains swinging in concert: cortical phase synchronization while playing guitar. BMC Neuroscience 2009, 10:22 doi:10.1186/1471-2202-10-22


How are these review-forgetting curve calculated? I saw quite some illustration about how reviewing helps remembering. Like:

SOURCE: http://www.mentormegate.com/wordpress/2014/06/10/mentor-me-gate-the-forgetting-curve/

I wonder how are these calculated? Are there reliable sources of the data?

While I can't speak about the specific graph in question, I can explain the process of obtaining an empirical estimate of a forgetting curve.

The basic process is (1) collect data; (2) model and graph data.

Collecting data

A standard design would involve a set of participants completing an initial learning exercise (e.g., a word list; a set foreign language words with meanings; a set of facts; etc.). Participants would then be given a recognition task to measure proportion of facts remembered (e.g., a recall task; a recognition task, etc.). The recognition task would then be repeated at various intervals (e.g., after a few minutes, a day, a week, a month).

Model and graphing

You could then graph mean performance (i.e., proportion correct) on the recognition task at each time point (i.e., baseline and various follow-up time points).

A typical forgetting curve involves a monotonic reduction in recall over time where the rate of forgetting slows and recall approaches an asymptote. See for example Averell and Heathcote (2011) for discussion of power and exponential functions of forgetting.

You could then use the lines of best fit to interpolate points between the measured time points.

Comments on review and forgetting curves

There is research that looks at the combination of practice and forgetting and the resulting memory consolidation that occurs through spaced practice. See for example Pavlik and Anderson (2005). The general finding is that (a) people forget over time; (b) revision restores recall; (c) forgetting is less after second and subsequent revisions.

Thus, the basic idea implied by the graph that spaced revision improves longer term recall is supported by research.

The smooth increase shown in the plot is incorrect. Presumably revision would be a relatively short and discrete event (i.e., perhaps 20 minutes) which leads to an abrupt increase in recall. Furthermore, the size of the gains achieved by repeated practice would depend on a range of other factors and may not be as great as implied by the graph.

References

Averell, L., & Heathcote, A. (2011). The form of the forgetting curve and the fate of memories. Journal of Mathematical Psychology, 55(1), 25-35.
Pavlik, P. I., & Anderson, J. R. (2005). Practice and Forgetting Effects on Vocabulary Memory: An Activation‐Based Model of the Spacing Effect. Cognitive Science, 29(4), 559-586.


How is fasting related to insomnia? Yesterday I started a new diet using intermittent fasting. For this reason I only ate one meal all day. I was pretty surprised how well I passed that day: I studied a lot, did some sports and fulfilled several programming exercises from university. After sports I had my first meal. Overall—a great day without any side effects from the intermittent fasting.

However, at 11 PM I went to bed. There I realized that I was not tired. So I read a book. One hour passed—still no feeling of fatigue. So, I thought, some push ups will make me tired. Nope, the push-ups did not work. It was already 1 AM, and I had to get up early. I decided to use my strongest means, which I only use before big exams: a glass of brandy. No effect! Meditation—nope. After that, 30 minutes of running outside in the cold—again, no effect. At 4 AM I decided to get up and study.

A weird experience. I know that I lack sleep; nevertheless, I can study and concentrate.

I Googled the keywords fastening and sleeplessness. Then I realized that it is a common pattern that some people sleep less during fasting.

Why is fasting related to insomnia?

Fasting causes stress and makes your body work off of fat rather than sugar. Sugar is of course related to insulin, which even in normal (non-diabetic) people must be maintained at a certain level (Kaditis et al., 2005). Without a proper level of insulin, your body will upregulate orexin in the brain until you eat (Willie, Chemelli, Sinton, & Yanagisawa, 2001). Orexin will give you artificial energy and inhibit sleep.

References

Kaditis, A. G., Alexopoulos, E. I., Damani, E., Karadonta, I., Kostadima, E., Tsolakidou, A., ... & Syrogiannopoulos, G. A. (2005). Obstructive sleep‐disordered breathing and fasting insulin levels in nonobese children. Pediatric Pulmonology, 40(6), 515–523.

Willie, J. T., Chemelli, R. M., Sinton, C. M., & Yanagisawa, M. (2001). To eat or to sleep? Orexin in the regulation of feeding and wakefulness. Annual Review of Neuroscience, 24(1), 429–458.


Are there any standard psychometric scales that are only applicable to within-subject designs? A while ago, I asked the question whether Presence questionnaires are valid in between-subject designs (see the question for the background to this assumption).

While the question garnered some encouraging feedback, no one seems to know the answer as of yet.

Example:
By way of a contrived example, I was suggesting that the situation would be similar were we to perform an experiment in which half the participants are told that they are to receive 1 litre of free beer, whereas the other half are told that they are given 10 litres of free beer.

If you asked all participants to rate their level of happiness at receiving the news that they are given said quantity of free beer, I think you would not see a difference (because free beer is free beer!).

However, if you were to repeat the experiment a second time with the same participants and now swapped the amount of beer between the two groups, I would expect people to lower their happiness ratings if their amount of beer got lowered, and up their ratings if their free beer levels went up. (NB: Participants do not actually receive free beer but are simply asked how happy the news of receiving free beer would make them, so they don't actually receive 1 litre instead of 10 or get 11 litres)

Question: So I'm wondering:
Are there any standard tests or phenomena that are, in a sense, meaningless when applied to between-subjects but work as a relative scale when applied to within-subjects experiments?

I think your intuitions are correct, and the reason is that Likert scales often suffer from poor construct validity.

One example that comes to mind is Alter et al. (2010), who use a mixed design, and note that participants in both conditions gravitate toward the middle of the scale on their first rating. They suggest that participants do not know how to use the scale at first; however, their second rating is informative because it can be compared to the first.

Several other studies (e.g. Dittrich et al., 2007; Olson et al. 2007) suggest that Likert scales are best used for relative rather than absolute judgments. Within-subject designs may abide by this rule because participants will implicitly use their previous ratings as anchors.

Although within-subject designs are often preferred, many times they are not feasible. (For instance, an experimental manipulation may make it impossible for a subject to be in both conditions without jeopardizing the effect of the manipulation). However, a properly designed scale may be usable in a between-subjects design. The key here is wording the question such that subjects will make judgements relative to some other criterion. So you may say something like:

"Compared to the last time you received one free beer, how happy were you upon receiving
 ten free beers?"

-5       -4       -3       -2       -1       0       1       2       3       4       5
less happy than last time      neither more or less happy     much happier than last time

This example is a little contrived--in fact it's not that great since the question is leading--but hopefully you get the idea.

Since you mention happiness, I will note that this issue has arisen in the happiness literature. Happiness is often assessed by a Likert scale, but the wording of the question
can evoke different comparative standards. For instance, Steffel & Oppenehimer (2009) report that people respond differently whether they think about intra- vs inter- personal happiness (i.e. "How happy are you compared to others?" vs "How happy are you compared to how happy you would like to be?") When left to their own accord, they typically adopt an inter-personal comparison. However it is best to make this comparison explicit whenever possible to avoid these issues.

  Alter, A. L., Oppenheimer, D. M., & Zemla, J. C. (2010). Missing the
  trees for the forest: A construal level account of the illusion of
  explanatory depth. Journal of personality and social psychology,
  99(3), 436. PDF

  Dittrich, R., Francis, B., Hatzinger, R., & Katzenbeisser, W. (2007).
  A paired comparison approach for the analysis of sets of Likert-scale
  responses. Statistical Modelling, 7(1), 3-28. PDF

  Olson, J. M., Goffin, R. D., & Haynes, G. A. (2007). Relative versus
  absolute measures of explicit attitudes: Implications for predicting
  diverse attitude-relevant criteria. Journal of Personality and Social
  Psychology; Journal of Personality and Social Psychology, 93(6), 907.

  Steffel, M., & Oppenheimer, D. M. (2009). Happy by what standard? The
  role of interpersonal and intrapersonal comparisons in ratings of
  happiness. Social indicators research, 92(1), 69-79.


Do my cats really know I exist? I wonder if my cat really knows me as an individual or just a mysterious connected object that somehow has hands and legs attached to a body. When I pet him, does he know that this action originates from my brain (head)? Or does he think that there is a mysterious soft massaging machine hanging in the air? Of course, most of us believe the former. Especially as he seems to be attentively looking into my eyes when I do so. But I wonder if there have been any rigorous scientific experiments verifying that? And from the Lex Fridman's interview of Christof Koch (47:47), he mentioned that bees have very complex neurons and can identify individuals. I also wonder how the experiment was done to verify that.

Although there is a robust science of animal behavior, it's very difficult to determine what kinds of experiences or thoughts animals are having. In short, we can only observe their behavior. Philosophers argue that a "zombie" or a robot could also demonstrate exactly the same behaviors but have no mind behind them, which means that we can't infer the thoughts just from the behaviors. We can't measure the thoughts themselves. Even neural activity is just a proxy; they are not the thoughts. Frans de Waal's recent bestseller goes into great depth on animal emotions and suggests that there are no uniquely human emotions; I'm guessing he would think that your cat understands you as an agent and has loving feelings towards you.  https://www.nytimes.com/2019/02/25/books/review/frans-de-waal-mamas-last-hug.html


How to import images used to analysis in SPM to FreeSurfer FreeSurfer uses the recon-all command to semi-automatically generate its statistics. This tool implies a certain directory structure in which the files with the images for the samples should be organized into. In FreeSurfer tutorial they call this specific directory structure the FSFAST structure.

I need to analyse images that were previously worked on in SPM, and it has the following directory structure for the patients:

/experiment/patients/A.o/

and for controls:

/experiment/controls/A.o/

Within each directory there are .hdr, .img, .mat and .mask files for each observation, which was obtained in two different times. So the naming of the files have the following order:

experiment_subjectnumber_time1.img

and for the second acquisition reads:

experiment_subjectnumber_time2.img

The same with all the before mentioned extensions (hdr, mat, mask).

It seems that in the FreeSurfer workflow the command unpacksdcmdir is used to extract data from the nii and dicon types and organize them in the FSFAST structure. Can it be used on directory structures like the one I have?

I found help at the FreeSurfer mailing list regarding this question. The answer is that for the structural analysis, there is no need to run the recon-all command in a specific directory structure.

It is just a matter of running

recon-all -s SUBJECTNAME -all -i IMAGE.IMG

Note that I am feeding an img file, which is what I am using now, however the creators of the software suggest the use of the DICON filetype.


Which brain areas are linked to Hyperactivity in ADHD? I'm looking for some research identifying which brain areas or biological processes are behind specifically the hyperactivity symptoms of ADHD? I have done a preliminary search but most of the research I have found is about general ADHD symptoms/ how the brain of an individual with ADHD is different I'm struggling to find stuff focusing on the hyperactivity aspect.

I think the studies that you were after have only recently been published earlier this year. 38 subjects with ADHD had fMRI scans and compared with a database. The study found that -

  More severe hyperactivity was associated with increased functional connectivity in the left putamen, right caudate nucleus, right central operculum and a portion of the right postcentral gyrus within the auditory/sensorimotor network.More severe hyperactivity was associated with increased functional connectivity in the left putamen, right caudate nucleus, right central operculum and a portion of the right postcentral gyrus within the auditory/sensorimotor network.
  https://bmcpsychiatry.biomedcentral.com/articles/10.1186/s12888-019-2031-9


Is it reasonable to have a factor with only two levels in a carry-over design for an fMRI study? I'm planning a carry-over design for an fMRI study.

To save time, since it seems that I'll need a huge number of trials for my purpose, I'm wondering if it's reasonable to have a matrix 2x3x3, meaning that one dimension has only 2 levels instead of 3 as the others do.

I'm not an expert in neuroimaging, so I had to search a little bit to learn about how carry-over designs apply to fMRI (I found Aguirre, 2007). Thus, feel free to correct me if there is something specific about this problem domain that influences the correct answer to this question.

However, based on general principles of experimental design of repeated measures experiments, you always have to choose

how many factors you want,
how many levels you want for each factor,
what levels you have for each factor, and
what factors you hold constant.

The particular levels you choose are directly tied to your research question. There are often trade-offs between the cost of resources required to have more experimentally manipulated levels and the benefit of additional questions that can be answered. Thus, I don't think a black and white answer can be given. You need to weigh up the pros and cons.

And presumably you have already made many experimental design decisions to get to this point. There's nothing magical about 3 levels to a factor. If anything, in experimental psychology two levels seems more common. And you could have four or five or more.

References

Aguirre, G.K. (2007). Continuous carry-over designs for fMRI. Neuroimage, 35, 1480-1494. HTML


What evidence is there that the adult brain can produce new neurons? At school I was taught that the adult brain did not produce new neurons. That we had the maximum number of neurons and this would only diminish over time due to events, like head injuries, drinking excessive quantities of alcohol, various other processes, not to mention the general atrophy the body experiences through the process of aging.

I remember sitting through a Neuroscience lecture (about 15 years ago), and learning, that studies had shown that whilst exercising enabled the brain to produce new neurons.

What is the latest evidence that the adult brain can produce new neurons?

Please note the link is not to the lecture I refer to.

For a comprehensive review, see:

Berg, D.A., Belnoue, L.,Song,H., Simon A. (2013) Neurotransmitter-mediated control of neurogenesis in the adult vertebrate brain.  Development, 140(12), 2548-2561. [DOI].

Briefly,

  active adult neurogenesis is confined to two distinct
  locations: the subventricular zone (SVZ) of the lateral ventricles in
  the forebrain; and the subgranular zone (SGZ) of the dentate gyrus
  (DG) in the hippocampus

These areas contain radial glial-like cells, which act as neural stem cells, and the growth of which is modulated by the respective neurotransmitters.  For example, cells which are GABAnergic will be modulated (enhanced in the SVZ and inhibited in the DG) via GABA that has diffused out of the synapses of neighboring cells

  GABA is released from parvalbumin-expressing interneurons in the adult dentate gyrus
  (DG) and inhibits the activation of quiescent RGLs through activation of the γ 2-subunit-containing GABA A
  receptor.

  In the SVZ, GABA also signals to and depolarizes neural
  progenitor cells, but the mechanism of release is different from that
  in the DG (Wang et al., 2003; Liu et al., 2005). Migrating
  neuroblasts release GABA in a non-synaptic, non-vesicular fashion,
  which tonically activates signaling in progenitor cells.

There are mechanisms through which the progenitor cells are stimulated that rely on neurotransmitters, but are not specific to cell subtype:

  Neurotransmitters control neurogenesis without subtype specificity. If NSCs have restricted potential, transmitters could act on both NSCs and/or amplifying populations.

It's still a complicated story, but the long and short of it is, in specific regions of the brain, adult neurogenesis is known to be possible and some of the neurotransmitter-based growth factors are now being elucidated.


Does the transcription method used (e.g., printing, handwriting, typing, voice recording, etc.) affect memory retention? When I was in high school, one of my teachers used to make us hand print copies of materials from transparencies on an overhead projector (I may be showing my age), with the reasoning that re-writing notes by hand was better for memory retention.

I later was told, via sources I can no longer recall, that typing out notes wasn't as good for memory retention because it was too easily done without thinking. Hand printed/written notes, I was told, were superior because they forced you to think about the words and letters being written, whereas typing uses more or less the same actions for each character and can be done faster with less conscious thought. Anecdotally, I know I certainly type faster than I write, and am better able to multitask as I do.

Is there any evidence to support the idea that writing is better for retention than typing?
Does it matter if you print or handwrite the transcription?
Do other transcription methods, such as dictating into an audio recording device, have better or worse retention rates?

A recent senior thesis by Schoen (2012) addressed this exact question. Students watched a filmed lecture and were randomly assigned to take notes with either by typing or handwriting. After the lecture, students were given a few distractor tasks, and then given a retention test. Other students were assigned to take notes from a textbook, instead of a lecture.
In contrast to your theory, there was a main effect of transcription method, such that typing notes led to better retention. However, there was an interaction with context, and it appears that there is no simple main effect for textbook notes. (see figure below)
One could posit that this interaction occurs because of the demands of the task. Taking notes by typing is easier and faster, i.e. more fluent. Hand-writing notes leads to higher cognitive load, which may lead to the student paying more attention to note-taking and less attention to the lecture itself. This would explain why textbook notes showed no effect. I only skimmed through the paper, but it seems very interesting and right to the point of your question, so I would suggest reading it for more info.

Additional information:
Before looking this up, I expected the opposite pattern. Bjork & Bjork (2009) have found
that creating desirable difficulties in learning can promote retention. For instance, it is well known that generating information, such as fill-in-the-blanks, promote better retention compared to, e.g., multiple choice tests. Diemand-Yauman, Oppenheimer, &  Vaughan (2010) have found that presenting study material in hard-to-read fonts leads to better encoding and retention of the material.
Similarly, a study by Yang, Gallo, & Beilock (2009) looked at the effect of motor fluency on retention. Subjects typed a two-letter dyad (such as ae or aq). Fluent dyads were letter pairs which were typed with two fingers; these pairs are typed faster and more easily than dyads that used the same finger because there is no motor bottleneck. Subjects were later given a recognition test to determine which dyads were presented to them. They found that subjects produced more false alarms for fluent dyads than disfluent dyads. This is particularly strange because false alarms, by their nature, were not actually typed by subject. This effect only held for expert typists, corroborating previous literature which suggests that fluency leads to false recognition. (Presumably for novice typists, none of the dyads were fluent enough to produce a higher level of false alarms).
So it seems there is a confluence of effects here. Disfluency--that is, making things more difficult--can promote deep processing and lead to better encoding and retention. However when this process causes one to neglect other information, such as paying attention to the lecture itself, retention suffers.
For additional reading on the effects of fluency on problem solving, I suggest Alter, Oppenheimer, Epley, & Eyre (2007) and Oppenheimer (2008).
From Schoen (2012):

Alter, A. L., Oppenheimer, D. M., Epley, N., & Eyre, R. N. (2007). Overcoming intuition: metacognitive difficulty activates analytic reasoning. Journal of Experimental Psychology: General, 136(4), 569. PDF
Bjork, E. L., & Bjork, R. (2009). Making things hard on yourself, but in a good way: Creating desirable difficulties to enhance learning. New York: Worth Publishers. PDF
Diemand-Yauman, C., Oppenheimer, D. M., & Vaughan, E. B. (2011). Fortune favors the Bold (and the Italicized): Effects of disfluency on educational outcomes. Cognition, 118(1), 111-115. PDF
Oppenheimer, D. M. (2008). The secret life of fluency. Trends in Cognitive Sciences, 12(6), 237-241. PDF
Schoen, I. (2012). Effects of Method and Context of Note-taking on Memory: Handwriting versus Typing in Lecture and Textbook-Reading Contexts. Pitzer Senior Theses. Paper 20. PDF
Yang, S. J., Gallo, D. A., & Beilock, S. L. (2009). Embodied memory judgments: a case of motor fluency. Journal of Experimental Psychology: Learning, Memory, and Cognition; Journal of Experimental Psychology: Learning, Memory, and Cognition, 35(5), 1359. PDF


What is the scientific definition of "brain training"? A lot of companies are selling products under the heading of "brain training", and "brain exercises", "brain games" such as Nintendo DS Brain Training, Lumosity, and a host of other companies.

I'm highly sceptical that such exercises have any generalised effect beyond improving the task that is being practiced and possibly some very limited form of generalisation. Nonetheless, I was curious about what makes an exercise or a program of activities "brain training".

What is the scientific definition of "brain training"?
Alternatively, what definitions have been proposed by researchers or very popular providers of brain training?

Such a definition would presumably make clear how daily living is different to brain training. It would also hopefully clarify whether daily cognitive activity like doing a crossword, answering a question on stack exchange, making a shopping list, or playing a computer game is brain training or not.

I think in most scientific contexts, "brain training" refers to working memory training. Scott Barry Kaufman wrote a nice article entitled In Defense of Working Memory Training. Hulme and Melby-Lervag wrote a meta-analysis about working memory training. They note that these exercises would not generalize to other mental skills such as reading comprehension, word decoding, and arithmetic. However, they did find that these exercises did improve short term verbal and visuospatial spatial working memory skills.

Kaufman argues that one should not dismiss working memory training as not improving intelligence. It may improve one aspect of intelligence (i.e. working memory). Note that according to may researchers, intelligence is comprised of many facts. Also, the age of people participating in brain training should be taken account. For example, very young people and very old people may benefit more than "normal age" people. Likewise, personality traits such as conscientiousness and neuroticism should be taken into account.

Kaufman also notes that mindfulness meditation and other "whole body" exercises would be more beneficial than specific working memory training exercises.

Sources

Is Working Memory Training Effective? A Meta-Analytic Review by Monica Melby-Lervåg
and Charles Hulme. Developmental Psychology © 2012 American Psychological Association
2013, Vol. 49, No. 2, 270–291.

A Dynamical Model of General Intelligence: The Positive Manifold of
Intelligence by Mutualism by Han L. J. van der Maas et al. Psychological Review
2006, Vol. 113, No. 4, 842–861.


Can we truly random choose which finger to raise by counting to 10 in your mind? If a test person is asked to raise one of his 10 fingers at a given signal, is the choice truly random if he counts in his mind from 1 to 10 and associates with each number one of his fingers? The 1 he associates with the left pink, the 2 with his left ring finger, 3 with his left middle finger, etc. So the test person starts to count, the experimenter gives him a signal, after which the test person raises the finger associated with the number he arrived at while counting. Let's suppose the signal is given at a random moment. Is the choice "in sync" with the random signal given?

In other words, if the experimenter records which finger is raised after each of a 1000 signals are given to a single person, will the experimenter see that each finger is raised the same number of times (more or less, because the number of signals given is finite; the more signals, the better you're getting at the real distribution)? So in the case of 1000 signals given to a test person will the experimenter record that each finger is raised about 100 times?

Or does the test person not make a choice at all?

I think your question ultimately is about whether people can or are able to behave like a uniform random number generator drawing numbers from 1 to 10.
I don't think the fact that the participant needs to raise a finger changes things much.

Note that there is a distinction between what people do, and what people are capable of. A lot of research suggests that people are not very good at simulating randomness. That said, one can think of strategies that would allow a person to simulate randomness more effectively (e.g., drawing on sources of random information in the environment, or even applying a formula similar to that used to sequentially generate numbers using random number generators).

The broad question has already been posed on the site:
How well can a human-generated "random number" be predicted?

I also note that a participant could just report sequentially 1,2,3..., 10, 1, ... This data would show 100 of each number for 1000 signals. Of course, this would exhibit structure that would not be present were each trial independent.


Are liars inclined to lie to themselves? Reading the famous quote of Oliver Sacks, can we draw conclusions about liars?

  "We speak not only to tell other people what we think, but to tell ourselves what we think. Speech is a part of thought." [Oliver Sacks]

If speech is part of thought, then maybe liars can begin making fallacious thoughts in the long run?

Is there scientific evidence that suggests that speech affects thinking, possibly in relation to (pathological) liars?

Although I cannot answer the question on lying, (self-)speech and thinking are intimately linked to each-other, and actually used in UX-design (e.g. Krahmer, 2004). He compared two different approaches of thinking-aloud. In other words, people are perfectly able to verbalize their thoughts and actually do so.
One of the approaches he compares is a proposal of Ericsson and Simon (1993). In their nice and brief paper, they discuss (and refer to) many scientific papers (e.g. cognitive scientific and psychological) where self-speech is used during problem solving. Moreover, it showed that self-speech is related to other variables that correspond to thoughts.

In their review, Ericsson and Simon (1993) found that [[...]] there seemed to be close correspondence between subjects’ thoughts and what information that they looked at--when subjects verbalized thoughts about objects in the environment they very frequently looked at them.

I must admit that self-speech in this way is only used as a methods of identifying cognitive processes, and is often a mandated task in the experiment. However, the fact that people are able to reflect on their thoughts, gives me reason to believe that they can do so unconsciously too. If someone could correct me or confirm this, I invite you to do so.


Where can I find stimuli for steady-state visually-evoked potentials? I am a student working on a project which deals with Steady State Visually-Evoked Potentials (SSVEP) Stimuator. Does anybody know where can I find stimuli (checkerboard or single graphic) as a video file? It's very difficult to find these files on the Internet. I am not allowed to use videos from youtube.

Researchers are often willing to share their stimuli. If you know of a paper that uses the same kind of stimuli that you want to use, you could try emailing the authors. A friendly request with a brief explanation of why you want the stimuli usually works.


Find volume of lesion mask I have drawn a lesion mask using FSLeyes on a T1-weighted image for MS patients. Is there tool to get the lesion volume from the mask?

Assuming your mask is in NIfTI format (nii or nii.gz extension), you can use the fslstats command line tool for that. Just type fslstats on the command line to see the help text for command syntax and arguments. For your specific case, you can use:

fslstats <input> -V

where <input> is the path to your mask NIfTI file. The returned numbers will be the mask volume in voxels and mm^3.

FSL install

Since you said you used FSLeyes to draw your mask, I'm assuming you have the full install of the FSL package as well. If not, see their wiki for instructions.


What's the major difference between mind and brain? I am preparing a presentation on "Mind Reading Computer", and all articles that I came across were focused on reading interpretations from brain through sensors. Articles like  this clearly show a distinction between them, but from an engineering perspective, I need scientific facts. Does "mind reading computer" imply "brain reading computer", or does the term "mind" have totally a different meaning in the context? Any help and facts relating to the topic will be highly appreciated!

Wikipedia is often a good place to start for basic questions like these. Wikipedia has separate pages devoted to the mind, the brain, and even the mind–body problem, which is one example of the many theoretical challenges implied by the distinctions between "mind" and "brain". Simply stated:

The brain is a physical organ. It's entirely possible that much of its structure has relatively little bearing on the nature of the mind. For instance, glial cells are more numerous than neuronal cells. Glial cells play a relatively more supportive function than neurons, the direct functions of which may be more closely related than glial cells' to the functions of what we consider to constitute the mind.
Wikipedia describes the mind as, "The set of cognitive faculties that enables consciousness, perception, thinking, judgement, and memory." Google offers this primary definition: "The element of a person that enables them to be aware of the world and their experiences, to think, and to feel; the faculty of consciousness and thought." Neither of these definitions directly necessitate a physical substrate such as the brain. However, The Free Dictionary's primary definition includes the phrase, "Originates in the brain." These differences belie the controversiality of the term itself, as does @KeeganKeplinger's helpful answer.
Wikipedia's mind page has a section dedicated to its relation to the brain. This section mentions the mind–brain problem, as well as three philosophical stances on the problem:

Materialism: briefly, that there is no valid distinction, and all mental activities have neural bases
Idealism: essentially that all physical objects and processes are truly mental in nature
Dualism: that the mind exists somewhat independently of the brain and body, possibly as an aspect or property of the spirit or soul

Thus a simple answer would be that "mind" does imply "brain" for many if not most audiences, but some may opine that these are different (though probably not totally different) entities. Arguably the best approach would be to tailor your word choice to suit whichever entity your computer concept proposes to read most directly.


Why is almost all therapy done as one-hour sessions weekly? It seems far too spread out to me. Why do we pause mid-conversation and wait seven days?

When my car needed repair after an accident, the bodyshop spent 25 man-hours on repair. They did that over the course of one week, which is good because my car is essential for my life. I can't function without it. But if my car had needed therapy, it would've taken 25 weeks (almost six months) to get fixed. I'd have taken my dangerously broken car to them and had them start checking damage, only to say "times up" an hour later and boot me out the door to use my broken car for another week.

Mental health is more complex and also more immediately essential to a person. Why then do we work on it at such a slow pace?

I've tried researching alternatives, and other than checking into full-time inpatient care, the other option is to find a therapist who can schedule more than one appointment per week, which is very rare. The therapists that have more than one open slot in their schedule at any time are the least well-regarded online. The well-reviewed ones have wait-lists to get a single appointment.

I understand that some therapy is a 'maintenance' model, where the patient only needs to talk about what happened since last session, but what about patients who have a long history to unpack, or are in the middle of a crisis? Why do we apply the weekly appointment model to those cases?

Why have therapists adopted this model? What is the rationale and history that led to it?

Q1 — Your Main Question — Why is almost all therapy done as one-hour sessions weekly?

The studies

Two studies attempted to observe the effects of session frequency in routine practice of psychoanalytic psychotherapy. Both relied on retrospective evaluations by patients after completing therapy, and on naturalistic data regarding session frequency and dose. Each was asked to rate his or her recovery in therapy, including decrease in symptom distress and increasein morale.

Both studies indicated a relationship between the frequency of sessions and patients’ perceptions of recovery, where patients being seen only once a week had less positive perceptions of their experience than patients being seen two times a week or more. In fact, positive perceptions of recovery were incrementally related with the frequency of sessions, with once a week indicating the least amount of recovery, twice a week somewhat more, and three times a week the most recovery in therapy (Freedman, Hoffenber, Vorus, & Frosch, 1999; Sandell et al., 2000). This provides some evidence that patients’ perceptions of their own recovery may be affected positively by increased session frequency.

A follow-up study to Sandell et al. (2000) found an interaction effect in long-term follow-up (i.e., 3 years, with measures taken each year) between duration and frequency, where outcome was better among the low frequency/low duration group and among the high frequency/high duration group (Sandell, Blomberg, & Lazar, 2002). These findings illustrate the potentially complex relationship between session frequency and other parameters, including the number of sessions and duration of the course of treatment; ultimately, they indicate that session frequency seems to be related not only to immediate perception of therapy, but to long-term outcome.

So what is this telling us?

Twice weekly or more sessions may gain quicker results in perception, but in the long term, it is doing the client a disservice.

The frequency of sessions helps balance cost, intensity, and emotional containment (Seeman, n.d.).  Therapy can be emotionally intense and someone may learn many things (about themselves and what they are dealing with) in session. More time in session can raise an amount of information which can be difficult to absorb mentally and emotionally, and this is what Sandell, Blomberg, & Lazar (2002) was starting to realise.

High frequency/high duration therapy as indicated by Sandell, Blomberg, & Lazar would be very costly, and, from my experience as a therapist who as part of training has had to undergo therapy too, would not be as beneficial as low frequency/low duration therapy.   With high frequency/high duration therapy, the client is not necessarily fully assimilating the information at their own pace, and, the chances are, the therapist is guiding too much on how to interpret the information raised in session. Low frequency/low duration therapy is about pacing your therapy, and the fact that therapy does not just happen in the room.

The time outside the room enables the client to assimilate the information which has been discussed in session at their own pace.  Depending on the form of therapy, the therapist may even set some "homework tasks" outside of the session which are optional, but may help with assimilation processes.

Being weekly, it will be recent enough that session continuity will be maintained.  Any longer in duration between sessions runs the risk of continuity problems as what was discussed can be hard to remember to a certain degree, and the flow of conversation and therapy can be upset slightly, affecting rapport.  There may be times when you may wish to cancel a scheduled appointment with your therapist because you are finding things too difficult.  That is fine as long as you give the pre-agreed notice to your therapist.  Late cancellations can incur cancellation charges with most therapists.

It is part of therapy in some cases to want to skip a session once in a while, and as long as there are not too many cancellations, your therapist will understand and can pick things up when you return, whilst examining with you what made things difficult.  If there are a lot of cancellations, questions will be raised as to whether you are ready for therapy. in order for therapy to work, the client needs to be ready for it

  Clients immersed in intense emotional or life changes may see their therapist twice a week or more often to help keep them be emotionally centered and assist them in activating coping skills (Seeman, n.d.)

however, once things have reached a certain point, it is better for the client to revert to once-weekly sessions for reasons already pointed out.

Q2 — Why do we pause mid-conversation and wait seven days?

With the idea of conversations being cut mid-way because of the end of session, a good therapist will manage the session and enable as smooth an ending as possible.  Although sessions booked will be an hour long, the typical “therapy hour” is 45 to 50 minutes.  In some situations a therapist may offer longer sessions. For instance, a couple in therapy may find themselves just getting into a long-needed conversation. Added time may help them maintain the momentum.

The 10 to 15 minute difference with the "therapy hour" enables therapy to be closed as smoothly as possible giving time for the client to transition from therapy session to life outside the room.  When you are approaching the end of the therapy hour, your therapist should be mindful of that and work towards a smooth closure of the session in order for the client not to be "left dangling with no support" after just talking about something very emotional without some kind of closure for the time being.

Further Reading

For tips on how to get the most out of Psychotherapy, see the webpage by Gary Seeman, PhD

For more information about what makes therapy work, see:

Duncan, B. L., Miller, S. D., Wampold, B. E., & Hubble, M. A. (2010). The heart and soul of change: Delivering what works in therapy. American Psychological Association.DOI: 10.1037/12075-000

References

Freedman, N., Hoffenberg, J. D., Vorus, N., & Frosch, A. (1999). The effectiveness of psychoanalytic psychotherapy: The role of treatment duration, frequency of sessions, and the therapeutic relationship. Journal of the American Psychoanalytic Association, 47(3), 741-772.DOI: 10.1177/00030651990470031001

Sandell, R., Blomberg, J., Lazar, A., Carlsson, J., Broberg, J., & Schubert, J. (2000). Varieties of long-term outcome among patients in psychoanalysis and long-term psychotherapy: A review of findings in the Stockholm outcome of psychoanalysis and psychotherapy project (STOPP). The International Journal of Psychoanalysis, 81(5), 921-942.No working DOI available[Free PDF available at: https://www.researchgate.net/publication/12217712_Varieties_of_long-term_outcome_among_patients_in_psychoanalysis_and_long-term_psychotherapy_-_A_review_of_findings_in_the_Stockholm_Outcome_of_Psychoanalysis_and_Psychotherapy_Project_STOPPP]

Sandell, R., Blomberg, J., & Lazar, A. (2002). Time matters: On temporal interactions in long-term follow-up of long-term psychotherapies. Psychotherapy Research, 12(1), 39-58.DOI: 10.1080/713869616

Seeman, G. (n.d.). Getting the Most Out of Psychotherapy [Online]Available at: https://drgaryseeman.com/getting-the-most-out-of-psychotherapy


Should psychological checks be as frequent as physical checks to evaluate a patient's condition? Are there differences between psychological and physical attributes that could justify the lack of these periodic tests in psychology?

ABSOLUTELY! The physical and mental are often connected. Take, for instance, the Thyriod. If the thyroid is physically unhealthy then it can cause mental disturbances. It can cause a slew of psychological manifestations for someone. When preceived by a psychological professional, they treat the symtoms they interpret and preceive from their paradigm they treat their patient with psychological techniques and medications.

I have seen this first hand where someone can exhibit pyschological disturbances and are incorrectly diagnosed because the psychological professional does not test their physical state.


Reducing adverse impact, discrimination and unfairness when using psychological assessments for selection purposes How can we reduce adverse impacts such as bias, discrimination, and unfairness when using cognitive ability tests and personality tests for selection purposes in an international context?

This is a big and important topic. The following is a bit of an introduction. Feel free to ask a separate more focussed question.

Some terminology

In general distinctions are made between the terms bias, fairness, and discrimination.

Bias is a statistical term. Bias for a group can indicate that test scores for that group are systematically lower or higher than would be expected from the group's true score. It is often assessed by seeing whether there is a group by test interaction in predicting the criterion. In particular, just because groups differ in means does not mean the test is biased, the groups may differ on the underlying construct.
Fairness is a moral and ethical construct. There is scope for different people to value different things. For example, using a test that while unbiased
, reduces the prevalence of a minority group, may still be seen as unfair. Likewise, affirmative action might be seen as fair in the context of a history of discrimination, yet others may perceive that is being unfair to the non-minority group.
Discrimination is often used in a legal sense to refer to either direct or indirect forms of discrimination.

Reviewing this area

I strongly recommend you read page 16.16 onwards (from the section labelled "Improved understanding of subgroup differences") of Sackett and Lieven's (2008, PDF) review.

In particular they note that several good predictors of task performance also show subgroup differences. Thus, there is sometimes a trade-off between validity and adverse impact. For a review of subgroup differences see Hough et al, 2001.

I quote a few sections with particular relevance to the question of what can be done to minimise adverse impact:

  Sackett et al. (2001) reviewed the cumulative evidence and concluded
  that several proposed mechanisms are not, in fact, effective in
  reducing differences. These include (a) using differential item
  functioning analysis to identify and remove items functioning
  differently by subgroup, (b) providing coaching programs (these may
  improve scores for all, but group differences remain), (c) providing
  more generous time limits (which appears to increase group
  differences, and (d ) altering test taking motivation.

  Sackett et al. (2001) did report some support for expanding the criterion as a means of
  reducing subgroup differences. The relative weight given to task,
  citizenship, and counterproductive behavior in forming a composite
  criterion affects the weight given to cognitive predictors. Sackett et
  al. cautioned against differential weighting of criteria solely as a
  means of inﬂuencing predictor subgroup differences; rather, they
  argued that criterion weights should reﬂect the relative emphasis the
  organization concludes is appropriate given its business strategy.
  They also reported some support for expanding the range of predictors
  used. The strategy of supplementing existing cognitive predictors with
  additional predictors outside the cognitive domain can reduce the
  overall subgroup differences in some circumstances. This strategy has
  received considerable attention because broadening the range of
  predictors has the potential to both reduce subgroup differences and increase validity

International context

If you're particularly interested in the international context check out Myors et al (2008) which provides an overview of the context of selection and adverse impact from the perspective of a wide range of different countries.

General thoughts

In general, there is also a  wide range of general strategies that we might recommend to increase fairness. e.g., Ensure that choice of selection tools is based on a thorough job analysis and an understanding of the competencies required for the job; Use well-validated measures; standardise decision making processes; minimise potential for cheating; etc.

References

Hough LM, Oswald FL, Ployhart RE. (2001). Determinants, detection and amelioration of adverse impact in personnel selection procedures: issues, evidence and lessons learned. International Journal Selection & Assessment. 9:152–94.
Myors, B., Lievens, F., Schollaert, E., Van Hoye, G., Cronshaw, S.F., Mladinic, A., Rodr\'\iguez, V., Aguinis, H., Steiner, D.D., Rolland, F. & others (2008). International perspectives on the legal environment for selection. Industrial and Organizational Psychology, 1, 206-246. PDF
Sackett PR, Devore CJ. 2001. Counterproductive behaviors at work. See Anderson et al. 2001,
pp. 145–64
Sackett, P.R. & Lievens, F. (2008). Personnel selection. Annu. Rev. Psychol., 59, 419-450. PDF


Pathological distress caused by being discouraged to say "thanks" on online communities The Stack Exchange network users are not encouraged to leave comments expressing thanks.

  Please do not add a comment on your question or on an answer to say "Thank you". Comments are meant for requesting clarification, leaving constructive criticism, or adding relevant but minor additional information – not for socializing. If you want to say "thank you," vote on or accept that person's answer, or simply pay it forward by providing a great answer to someone else's question.

Given some people are taught from a preschool age to express thanks and this practice is reinforced throughout a lifetime. So coming to an online community can be difficult for some people not to express thanks.

What is happening psychologically when an individual has immense discomfort (to a point of preferring the discomfort of not complying with the wishes of an online community), that is almost compulsive in having to continue with an instilled social habit, such as expressing thanks.

Nb To me, it could be related to cognitive-dissonance, but this doesn't seem to be the correct term.

DISCLAIMER: I do not have any official education in cognitive sciences.

Maybe problem is not in saying "thank you", for me upvoting is very close to saying thank you.
I think it is rather obvious what are benefits from discouraging "thank you", it would be hard to find real content in "thanks forest".

Perhaps people wish that receiver knows who said thank you

I Joe want Marc to know that 'I, Joe' am thankful.


How can higher concepts get unrolled with upward and feedback connections differing? In the neocortex, input patterns are compressed hierarchically. Sensory inputs in the lower levels are combined by higher levels to form abstract concepts. However, there are even more feedback connections ranging from higher levels downward to lower ones. Those are assumed to unroll higher concepts back into lower patterns that could have caused them in the first place.

If patterns could flow up and down through the same synapses, it would be easy to understand how higher patterns cause lower patterns similar to those that could have caused them. In a mathematical sense, traversing the connections in the inverse direction would cause the inverse of the upward transformation.

But synapses are mainly directed. So patterns cannot flow downward through the same synapses. How do the feedback connections still learn transformations similar to the inverse of the upward connections?

Caveats

There's some points to keep in mind when thinking about this:

While it is true that connections in cortex are reciprocal, this does not mean that they are symmetric. Cortical connectivity is quite elaborate and the neurons that send bottom-up signals to the next higher area are not necessarily the same neurons that receive the feedback. The forward signals seem to originate mostly from cortical layers 2/3 and 5, whereas the targets of feedback are primarily layers 1 and 6 (see for example Roelfsema & Holtmaat (2018) figure 2 and Shipp (2007)). On the other hand, an axon that terminates in layer 1 may be contacting dendrites of neurons with cell bodies in other layers, so the story is not that simple (see Larkum et al. (2018)).
The connections may not be monosynaptic. Many of the communication between cortical areas happens via the thalamus and other subcortical structures (see the same papers as in the last point).

Learning symmetric connections

I will ignore these two points for now and just assume that a set of neurons in a lower-level cortical area (for example, V1) and a set of neurons in a higher-level cortical area (let's say V2) have reciprocal, monosynaptic connections. So how can a neuron $y_j$ in V2 ensure that its feedback to V1 generates roughly the pattern that excited $y_j$ in the first place? One possibility is to use Hebbian learning. Essentially, if synaptic strength $w_{ji}$ in the forward and $w_{ij}$ in the feedback pathway both grow when $x_i$ in V1 and $y_j$ in V2 fire synchronously / with strong rates, the connections will tend to become symmetric over time.

Instar-outstar learning

Pure Hebbian learning ($\Delta w_{ji} \propto x_i \cdot y_j$) tends to be unstable, so one needs to add a decay term to the weights. This way you arrive at instar-outstar learning (see for example Grossberg (2013), section 1.5), which has been used for exactly this purpose: learning appropriate connections between higher-level categories and lower-level inputs.

The forward connection would perform instar learning ($\Delta w_{ji} \propto y_j \cdot (x_i - w_{ji})$). This means that the weights of all synapses going into neuron $y_j$ compete. Over time, $w_{ji}$ will tend to the mean input vector $\langle \mathbf{x} \rangle$.

The feedback connection would perform outstar learning ($\Delta w_{ji} \propto x_i \cdot (y_j - w_{ji})$). This means that the weights of all synapses going out of neuron $y_j$ are in competition. Note that this may be difficult to implement in a biological neural network, since it means that synapses on different neurons $x_i$ have to compete with each other. Over time, $w_{ij}$ will also tend to the mean output vector $\langle \mathbf{x} \rangle$. Since the input of the forward connection is the output of the feedback connection are identical, the weight vectors should become symmetric.

Oja learning

Note however, that this means the weight matrices are transposes of each other, not inverses. Also, you would need to ensure that different neurons in V2 do not all learn the same pattern, for example by inhibitory connections between them.

One way to overcome both of these problems is to use the Oja subspace rule (see Oja (1992, 1997)): $\Delta \mathbf{W}_{ji} \propto (\mathbf{x} - \mathbf{W} \cdot \mathbf{y}) \cdot \mathbf{y}^T $ This rule ensures that the weight matrix is orthogonal, so that the transpose will be an inverse. However, note that this involves some more competition between synapses on different neurons, so it is not biologically plausible. Note also that the weight vectors will now tend to principle components of the input patterns, not to mean values.

Beyond the simple scenario

These learning rules make it possible to learn symmetric connections in a very simple scenario, assuming directly connected, rate-based neurons. The proofs to show that instar-outstart approximates the mean and Oja's rule performs PCA also assume linear neurons, which is a further simplification. So coming back to the caveats above, in cortex the story is probably not so simple. Still, these principles (Hebbian learning with competition in both directions) may provide the basis for an explanation.

For example, despite caveat 1 Hebbian learning may still be useful since neurons across all layers of a cortical column tend to respond to the same stimuli. So as long as the rates are similar enough, the connections could still learn to be somewhat symmetrical or at least to have the kind of concept unrolling function you have in mind.

Also, while I only talked about rate-based networks, something similar may work for spiking networks as well (see Clopath et al (2010) for a spike-time dependent plasticity rule that can lead to the formation of reciprocal connections).

TL;DR

Connections in cortex may not be directly symmetrical. Making several simplifying assumptions, it is possible to learn symmetrical connections with variants of Hebbian learning.

References

Clopath et al. (2010). Nature Neuroscience 13(3), 344-352. link
Grossberg (2013). Neural Networks 37, 1-47. link
Larkum et al. (2018). Frontiers in Neuroanatomy 12, 56. link
Oja (1992). Neural Networks 5(6), 927-935. link
Oja (1997). Neurocomputing 17, 25-45. link
Roelfsema & Holtmaat (2018). Nature Reviews Neuroscience 19(3), 166-180. link
Shipp (2007). Current Biology 17(12), R443-R449. link


What is the equivalent of a Hamming network in the NEF? After doing a bit of research, I'm somewhat convinced that Hamming networks are networks that classify, but only put out a single result, as opposed to other networks which output multiple results. In this case, is the equivalent in terms of the NEF a classifier (measuring similarity with a dot product between two vectors) followed by an associative memory?

An Associative Memory is a classifier and is equivalent to a Hamming Network.

For documentation on the NEF Associative Memory, see this practical Nengo documentation and the paper "A biologically realistic cleanup memory: Autoassociation in spiking neurons". Basically, each ensemble of an associative memory computes the similarity measure of the input firing pattern to a given firing pattern. Mutual inhibition is then used between the nodes to find the most similar input so that only the ensemble with the most similar input outputs a signal. In an associative, this output similarity signal is used to map the input pattern to a new output pattern.

A Hamming Network is a classifier that receives patterns with input nodes also detecting similarity. However, unlike the Associative Memory it has a binary output using mutual inhibition. That being said, it would be easy to add a thresholding ensemble to the output of the Associative Memory to accomplish this.

In conclusion, an Associative Memory is basically a Hamming Network implemented using the NEF.


Have there been any mechanisms proposed for normalization in probabilistic population codes? I heard a talk yesterday by Dora Angelaki about multi-sensory integration.  Part of the talk was about bayesian inference with multiple noisy sources of information.  I know that there has been a lot of theoretical work done on bayesian inference and population coding, but I was wondering if there have been any biological mechanisms proposed for the population activity normalization necessary for these computations?

It depends what you mean by a biological mechanism. If you mean that there should be a protein cascade that implements normalization, that doesn't seem plausible, in my opinion. Normalization in probabilistic population codes is just one of many computations that can be performed in a neural system.

If you're okay with the notion that there's nothing biologically unique about normalization, then Normalization for probabilistic inference with neurons (a paper written by my supervisor, Chris Eliasmith) proposes a spiking neural network performs normalization on probability density functions.


Can Transcranial Magnetic Stimulation (TMS), or a magnets cap make you smarter? According to wikipedia, TMS is a bunch of magnetic fields directed to the brain which stimulates and activates neurons.

If I wear a cap full of magnets, will it stimulate my neurons?
If yes, will a cap of magnets make me "smarter"?

Short answer
A cap of magnets, or state-of-the-art TMS protocols, will not make you smarter.

Background
First off, TMS uses bursts of magnetic stimulation in the order of milliseconds (Rothkegel et al., 2010). Pulses of magnetic stimulation are used, because permanent magnetic fields will not induce current flow. Hence, wearing a cap of permanent magnets will not do the job.

TMS can be used using single pulses to evoke motoric muscle twitches when applied to the motor cortex, or to evoke phosphenes when applied over the visual cortex (Thut et al., 2003). In the clinic, typically repetitive TMS (rTMS) is used, where the subject is exposed to trains of TMS pulses (Horvath et al., 2010). rTMS is nowadays approved to treat depression. A popular description says it 'activates neurons' in the prefrontal cortex (ABC News), but a more realistic view is to say that nobody knows why it works, and whether it works (National Institute of Health). It's also been investigated to treat psychoses or to decrease ear ringing (tinnitus).

Hence, TMS is generally applied to disrupt ongoing neural activity, i.e. to remove something. Indeed, TMS is typically associated with a disruption of function. For example, visual task performance is decreased when folks are subjected to TMS pulses (Thut et al., 2003). Hence TMS is not applied to add or enhance brain functions, let alone higher cognitive functions that govern intelligence.

References
- Horvath et al., J Vis Exp (2010); 45: 2345
- Rothkegel et al., Clin Neurophysiol (2010); 121(11):1915-21
- Thut et al., Clin Neurophysiol (2003); 114(11): 2071–80


How well defined is ADD/ADHD? I understand ADHD is a standard term, but I'm still a bit suspicious that it's not a useful one; Psychiatry doesn't seem like the most reliable field.

Are there good reasons for picking out the behaviors associated with ADHD and giving them a name?

Potential answers

Behaviors associated with ADHD strongly cluster
Analyzing
questionnaires of attention and focus behaviors with factor analysis
naturally produces an 'ADHD dimension' that explains a lot of
variance (similar methodology to identifying Big 5 personality
traits).
ADHD diagnosis is a strong independent predictor of something
interesting: income or grades or some contrived but interesting lab
test (controlling for obvious things like IQ)
Something else along these lines.

Like all psychiatric disorers, ADD and ADHD are diagnosed using a set of criteria listed in the Diagnostic and Statistical Manual of Mental Disorders, or DSM

The latest version is the DSM-IV-TR. The DSM-V is due out in 2013 and may change these criteria.

Diagnosis is expected to be done by a licensed professional who is able to assess these criteria.

From http://www.mental-health-today.com/add/dsm.htm :

INATTENTION
(need 6 of 9)

- often fails to give close attention to details or makes careless mistakes in schoolwork, work or other activities
- often has difficulty sustaining attention in tasks or play activities
- often does not seem to listen when spoken to directly
- often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (no if oppositional behavior or doesn’t understand instructions)
- often has difficulty organizing tasks and activities
- often avoids, dislikes, or is reluctant to engage in tasks or activities that require sustained mental effort (such as schoolwork or homework)
- often loses things necessary for tasks or activities (e.g., toys, school assignments, pencils, books, or tools)
- often easily distracted by extraneous stimuli
- often forgetful in daily activities

HYPERACTIVITY-IMPULSIVITY
(need 6 of 9)

- often fidgets with hands or feet or squirms in seat
- often leaves seat in classroom or in other situations in which remaining seated is expected
- often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness)
- often has difficulty playing or engaging in leisure activities quietly
- is often "on the go" or often acts as if "driven by a motor"
- often talks excessively
- often blurts out answers before questions have been completed
- often has difficulty awaiting turn
- often interrupts or intrudes on others (e.g., butts into conversations or games)

REQUIREMENTS

- Present at least 6 months, maladaptive and inconsistent with development level
- Some symptoms that caused impairment were present before age 7
- Some impairment from the symptoms is present in two or more settings (e.g., at school {or work} and at home)
- There must be clear evidence of clinically significant impairment in social, academic or occupational functioning


How can I determine which of Brainwave is dominant as one state by EEG data? I am a student working on EEGs.
I have a EEG data of Brainwave in 4 emotional states, namely anger, sorrow, joy and pleasure. Is there any method for determining the difference between these emotional states by analyzing the 5 Brainwaves (gamma to delta)? And how can I detect which brainwaves are dominant?

Each "brainwave" is a range of frequencies that make up the signal, usually called a frequency band (ie. "the gamma frequency band"). To determine differences between bands, you would generally look at the power spectral density (PSD) of the signal. For instance, you may want to compare the average power in each frequency band.

In practice the PSD is estimated by calculating a periodogram.


What is the most unified functional model of the hippocampus? There are many different incremental models of the hippocampus and it's role in learning as shown by a quick search. However, have there been any efforts to combine these various models into a single unified functional model?

I myself have not come across a complete end-to-end hippocampal model, but I would imagine that such an implementation would be quite broad in scope. Edmund Rolls has some nice papers on the hippocampus, one of which is a particularly informative and recent review:

Kesner RP, and Rolls ET. A computational theory of hippocampal function, and tests of the theory: New developments. Neuroscience and Biobehavioral Reviews 48 (2015) 92-147 PDF here (Second page missing?)

I'll be very interested to read other answers to your question.


What are the benefits of dyslexia? Reading the Wikipedia article on Dyslexia, it sounds very negative. The article defines Dyslexia as a learning disability, which I understand it is classified as. However, knowing individuals with dyslexia, they do not consider themselves to have a disability, they say that their brains process information differently. Not worse, just differently. And I can attest to the fact that some of the people I know who are Dyslexic far exceed my abilities in certain areas, namely music, picture / visual / spacial skills, memory, timing, etc.

The Wikipedia article mentions no benefits to dyslexia.

Have any studies been done on benefits of dyslexia?
If so, what were the findings ?

This is not my area, but I did a little research and found a few things:

Silverman (2000) has an interesting article discussing children who are gifted but also have a learning disability. The article makes a number of interesting points about how other skills are often developed in order to compensate for a given disability (e.g., like how people who are vision impaired are better able to use their remaining senses).

In relation to dyslexia, Silverman summarises the work of Ron Davis. Specifically, Silverman  stated that:

  Ron Davis (1994), in The Gift of Dyslexia, describes the benefits of
  dyslexia. He lists the basic abilities that all dyslexics share:

  They can utilize the brain’s ability to alter and create perceptions (the primary ability).
  They are highly aware of the environment.
  They are more curious than average.
  They think mainly in pictures instead of words.
  They are highly intuitive and insightful.
  They think and perceive multi-dimensionally (using all the senses).
  They can experience thought as reality.
  They have vivid imaginations. (p. 5)

That said, I haven't read the book, and I'm unclear on the degree of empirical support for these claims.

References

Davis, R. D. (with E. M. Braun). (1994). The gift of dyslexia. Burlingame, CA:
Ability Workshop Press.
Silverman, L. (2000). The two-edged sword of compensation: How the
gifted cope with learning disabilities. In Uniquely gifted: Identifying
and meeting the needs of twice exceptional learners, pages 153-159. FREE PDF


Reference request for creator of heuristic for processing fMRI data (T.Nichols) I am using nilearn and nipy package for python processing FMRI data. When computing mask, it says:

  Compute and write the mask of an image based on the grey level This is based on an heuristic proposed by T.Nichols: find the least dense point of the histogram, between fractions m and M of the total image histogram.

and

  This is based on an heuristic proposed by T.Nichols: find the least dense point of the histogram, between fractions lower_cutoff and upper_cutoff of the total image histogram.

In both masking functions of nilearn and nipy. Who is T.Nichols? I wasn't able to google him/her out.

here are the links to the functions:

http://nipy.org/nipy/stable/api/generated/nipy.labs.mask.html

https://nilearn.github.io/building_blocks/generated/nilearn.masking.compute_epi_mask.html

I know very little about fmri, but as @strongbad points out, surely it is Professor Thomas Nichols at Warwick.

I'm not sure what the authoritative reference is, but Luo and Nichols (2003) might be worth a look. They state:

  We construct a histogram based on all non-tail data (10th to 90th percentile) and use the location of the minimum bin as the antimode estimate.

Luo, W. L., & Nichols, T. E. (2003). Diagnosis and exploration of massively univariate neuroimaging models. NeuroImage, 19(3), 1014-1032. http://www-personal.umich.edu/~nichols/Docs/fMRIvis.pdf


Is it possible to permanently improve long-term memory? Many similar questions here ask either about working or short-term memory, or about various tricks and techniques to efficiently remember information. My question is, is it possible to improve the capability for remembering long-term itself? So that learning/memorizing something would take less time or repetition, and the acquired knowledge/information will be stored for longer and with less distortions.

The effect might not be permanent, but it should be prolonged and substantial. To illustrate my point, let's assume for argument's sake that learning poems has the effect of improving long-term memory. This would mean that, after regularly memorizing new poems for several weeks, i find that i'm able to memorize new poems spending less time, the poems retain remembered for longer. I'm also able to remember content of non-fiction and fiction texts better too, so that i can recall tricky facts and logical inferences, which before memorizing poems i tended to forget. So, is there a method to improve the general efficiency of your long-term memory? In other words, ability to retain more information for longer periods with less effort?

This is what I do to store something in the long term memory.

1) Place it in the short term memory (those methods depend on the material).

Use mnemonic memory techniques.
Repeat the facts in different order.
Relate the facts to something that you already know.
Organize the facts in a logical order (order improves memory).
Try to find semantic meaning the facts.
Practice with active learning methods like writing and talking rather than with passive learning methods like listening and seeing.
Make the learning experience engaging. Get involved with different activities that include using the material you have learnt. For example, teach it to others.
Draw a vivid mind map of what you learnt.
Jot down self questions on the material you had to remember.

2) Take a 10 minute break.
Answer the test that you designed and the mind map that you drew in step 1, all from memory.
Repeat step 1 for the facts which are the answers to the questions that you didn't answer correctly in step 1.

3) The day after. Do another repetition.
Repeat what you didn't in step 2. This time mark the questions to your test that weren't answered correctly.
During the month, every day, try to answer the questions that were marked as wrong by the previous day.
So for example, if in day 3 you didn't answer right to question 4,6,8.. mark them and repeat only them on day 4. If you answered question question 4 and 8 correctly and 6 incorrectly, mark question 6 as wrong. Repeat the process every next day, until all the questions are right, then stop the process.

4) The next month from the day you started step 3.
Repeat step 1-3. First, answer all the questions in your test, then make a general repetition. Design a new test..answer with the same technique described in step 3 to eliminate memory fading after the revision.

5) After half a year repeat step 4.

Just to add. I memorize dictionaries using this technique. If you have a lot of meaningless data to memories (dictionaries, encyclopedia, lexicons, fact books), you need a technique like mine, because most of the other techniques out there are too passive.

My technique also trains the memory better. It helps you to transfer memory from short term to long term (Especially the mnemonic techniques). The example that you bring relates to the idea of familiarity and semantic meaning. If you memorize English words, overtime it would be easier to memorize more English words than, let's say, french words.
It does only increase long term memory for a specific topic, not for everything.

Other factors that help to improve your long term memory are amount of sleep, physical health and nutrition.

References:

Tony Buzon. Memory books.
Introduction to psychology book  (A-level). Cognitive psychology chapter.
Self-study skills gained through university.

Semantic memory might be the reason you find it easier to remember more and more poems as you continue reading them.

Some research:
Semantic memory - http://www.sciencedirect.com/science/article/pii/S0022537173800568


Is the Thatcher Face Illusion only limited to face recognition? The so called Thatcher-Illusion has been documented not  only on humans but also in some monkeys.

However I can't find literature clearing out if this effect only applies to face-recognition.

What about familiar but non-face visual objects?

Perhaps in other cases the illusion has a different name?

It also seems related to the so called Picasso Problem.

Boutsen et al. (2006) seem to dig deeper but the paper has restricted access.

A proper answer should probably take into account the Fusiform face area

Short answer
According to a study by Boutsen et al. Thatcherization of objects (houses in this study) did not reveal the Thatcher effect, while faces did.

Background
The Thatcher-face illusion (Fig 1) is, in my opinion, not really an illusion. Instead, it is a phenomenon where in-congruent features are more apparent when observed in their normal everyday context and orientation. In Fig. 1, for example, ms Spears appears normal, but upside down in the left panel, while her face appears hugely distorted when the left panel is turned upside down.

Your question whether this also occurs in objects other than faces. According to a study by Boutsen et al. (2006), it doesn't. Boutsen et al. manipulated images of faces and houses. Houses did not show effects of thatcherization. The authors discuss the why behind this finding and mention that a number of factors may explain the lesser salience in objects, namely a higher variability in the number of manipulated house features and  their perceptual salience or relevance. Because of their more stable feature structure and configuration, inversion of house elements was thought to be less salient with houses than with houses. Unlike the parts of a building, facial features are highly relevant to an observer to determine identity or expression, thereby rendering configural manipulations of buildings less disruptive.

Fig. 1. Thatcher illusion of Britney

Fig. 2. Thatcherized face and house. source: Boutsen et al., 2006)

Reference
- Boutsen et al., NeuroImage (2006); 32: 352 – 67


How do neuro transmitters interact with neurons in the brain? I think emotions and hormones frames the overall thinking processes of the brain. However, I'm interested in how this works on a neuronal level. For example, dopamine is some kind of reward signal for the brain. How does it interact with individual neurons or synapses and affect the way they behave?

Actually it's a bit complicated but in simple terms :

Neurotransmitters are stored in a synapse in synaptic vesicles, clustered beneath the membrane in the axon terminal located at the presynaptic side of the synapse. Neurotransmitters are released into and diffused across the synaptic cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.

Most neurotransmitters are about the size of a single amino acid, however, some neurotransmitters may be the size of larger proteins or peptides. A released neurotransmitter is typically available in the synaptic cleft for a short time before it is metabolized by enzymes, pulled back into the presynaptic neuron through reuptake, or bound to a postsynaptic receptor. Nevertheless, short-term exposure of the receptor to a neurotransmitter is typically sufficient for causing a postsynaptic response by way of synaptic transmission.

In response to a threshold action potential or graded electrical potential, a neurotransmitter is released at the presynaptic terminal. Low level "baseline" release also occurs without electrical stimulation. The released neurotransmitter may then move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an inhibitory or excitatory way. This neuron may be connected to many more neurons, and if the total of excitatory influences are greater than those of inhibitory influences, the neuron will also "fire". Ultimately it will create a new action potential at its axon hillock to release neurotransmitters and pass on the information to yet another neighboring neuron.


How do the motor system and Central Pattern Generators interact? Central Pattern Generators are populations of neurons found in the spinal chord that assist in the creation of rhythmic movements. See "Human spinal locomotor control is based on flexibly organized burst generators" by Danner et al, for a recent publication on the topic. How does the brain-based motor system interact with these pattern generators? Do they operate mostly independently or is there some feedback being communicated? If there is feedback, what type of information is it transmitting?

Descending inputs onto the central pattern generating circuit provide stimulus in the form of neuromodulatory chemicals and synaptic currents (Marder 2012). The leech heartbeat pacemaker and the stomatogastric ganglion in crustaceans are well-studied model systems that show descending input from higher functions.

Specifically, in humans, we are not sure. This type of question is best answered in invertebrates for the time being. In invertebrate electrophysiology, the circuit can be "decentralized," by chemically or physically destroying the inputs from the ascending ganglia. In the stomatogastric ganglion, this results in a less-stable but still very robust central pattern (Hamood et al., 2015).


Controlling for response bias in a forced choice memory task I want to present participants a pair of items $a$ and $b$, each with an association $x$ or $y$. Later on participants will presented with the items singularly, and asked  'what was the association?'.  I'm interested in differences in their memory for the association, between levels of the association.

As I've specified it there is no way to separate differences in memory performance between levels from response bias, because being incorrect on association $x$ means that another response for association $y$ is recorded.  Signal detection methods seem to give me an overall measure of discriminability between the two and bias, but can't tell me if the bias is due to genuinely improved memory for $x$, or simply a predisposition to respond $x$.

What is the best way to deal with this?

Initial thoughts: I'm considering including previously unseen elements into the memory task and getting a measure of response bias that way.

Here is some random example data to help with thinking:

choice X | X    choice Y | X   choice Y | Y   choice X | Y
   18               18         18              18
   24               12         18              18
   30                6         14              22
   29                7         14              22

Let's start with signal detection methods. The big one in memory literature is D-Prime analysis (hits versus false alarms). If the subject chooses X more times than Y, you can compare the number of times choice X is made correctly versus chosen incorrectly (as a false alarm). If that was your paradigm, then choice Y would be the correct rejection (if correct) or a miss (if incorrect).

With this in mind, you can add some degree of confidence to your paradigm. Instead of only two choices, x or y, you can give for options (1 - definitely x, 2 - probably x, 3 - probably y, 4 - definitely y). Never give the option to say, I don't know, because subjects can be unaware that he or she knows the answer, and studies show subjects can be greater than chance through unconscious recognition. Then, if you're afraid of a side bias, extracting only "definitely" answers should be a way of excluding that possibility, because if they were just guessing they would choose the "probably" answers.