Which personality theories do belong to humanistic? I went through literature and I am confused which theories of personality belong to humanistic, in literature there is often just Rogers (who is sometimes also considered to be phenomenologic) and Maslow. Do you know about some other that could be considered for humanistic too?
Can I say that all humanistic psychologists created humanistic personality theory (e. g. Allport, Frankl etc.)?

TLDR: All humanistic psychologists helped to shape todays overall humanistic personality theory "(e.g. Allport, Frankl etc.)"

In order to enable a full grasp of the subject, I need to go over a few things, and to a degree, I am revisiting a few areas I covered in other answers to questions.  In fact, mentioning Gordon Allport in your question made me find something out which changes a few things in my past research.  You got an upvote from me with that.

First, a bit of history

As I pointed out in Why has behaviourism fallen out of favour?, there are what is known as 3 forces of psychology

  Behavioural Theory (First Force) – (Short & Thomas, 2014, p. 203)
  Psychodynamic Theory (Second Force) – (Short & Thomas, 2014, p. 139)
  Humanistic Theory (Third Force) – (Short & Thomas, 2014, p. 79)

Although there is now talk of a possible fourth force such as Multicultural Psychology or Transpersonal Psychology

The humanistic approach is said to have been fully developed in the 1950s through a meeting between Abraham Maslow, Carl Rogers and Clark Moustakas; and the underpinning philosophy of humanistic thinking is that, in the view of Maslow (1968, p. 10), psychoanalysis attends to the ‘sick’ half of therapy – disorder and treatment – whilst humanistic therapy tends to the ‘healthy’ half – growth, potential and self-actualisation. (Reeves, 2013).  However, the discussion regarding Humanistic Psychology was started a lot earlier than that by Gordon Allport in 1930 (see below).

Humanistic models of approach include (Counselling Directory, n.d.):

Existential Therapy,
Gestalt Therapy,
Human Givens Psychotherapy,
Person-Centred Therapy (PCT),
Psychosynthesis,
Reality Therapy,
Solution-focused Brief Therapy,
Transactional Analysis (TA), and
Transpersonal Psychology

All the founders of the above therapies (including Eric Berne) helped form Humanistic Psychology.

As my first link indicated, Behaviourism hasn't completely fallen out of favour. Due to the work of Carl Rogers, there has been some shift, although not a complete shift, away from the rigidity of the Psychodynamic approach towards the Humanistic approach to therapy and Behaviourism has also started to gain more of the spotlight again.

The key concepts of Person-Centred Counselling, Transactional Analysis and Gestalt Therapy are three of the most widely practiced. (Reeves, 2013)

According to Dr. David R. Hiles of De Montfort University, Leicester, England, the Pioneers of Humanistic-Existential Psychology include:

Carl Jung (1875-1961)

  Carl Jung is possibly one of the most important figures in psychology, and yet he remains controversial. For many psychologists he is little more than a historical curiosity. Someone who worked with Freud in the early days of the founding of psychoanalysis, and then went his own way, founded his own school of psychology, became rather eccentric, and is worthy of only the most cursory of mentions in introductory text books. To other psychologists, he is possibly the most complete psychologist that there has ever been.

Rollo May (1909-1994)

  Rollo May, the distinguished existential psychologist and existential psychotherapist, was a co-founder of the Humanistic Psychology movement. He was an outspoken critic of his contemporaries, and was largely responsible for integrating the humanistic and existential traditions.

Abraham Maslow (1908-1970)

  Maslow was a major American psychologist, a visionary, an inspired thinker, who radically altered the course of development of the discipline of psychology. Born in New York, he was educated at the University of Wisconsin, where he studied primate behaviour under Harry Harlow and Clark Hull. He returned to New York in 1935 by accepting a research position with Edward Thorndike at Columbia University. Through his contact with the New School for Social Research, near Greenwich Village, he came to know and study with:- Alfred Adler, Erich Fromm, Karen Horney of the psychoanalytic school; Kurt Goldstein, Max Wertheimer and Kurt Koffka of the Gestalt school of thought.

Frederick (Fritz) Perls, the founder of Gestalt psychology, is also on the list (see below).

Carl Rogers (1902-1987)

  Rogers pioneered the development of client-centred therapy. A major figure in the history of psychology, with a basically optimistic view of humankind, he was a co-founder of the Humanistic Psychology movement.

James Bugental (1915- )

  James Bugental is an important figure in the early development of humanistic psychology, and in the practice of a humanistic approach to psychotherapy.

Erich Fromm (1900-1980)

  Erich Fromm was a German psychoanalyst and social theorist, who always saw himself as neo-Frudian in orientation, but who many regard as having occupied a key position on the periphery of the humanistic movement.

Roberto Assagioli (1888-1974)

  Assagioli was an Italian psychiatrist and founder of Psychosynthesis. He trained as a psychoanalyst and was a member of the Freud Society in Zurich. He withdrew from membership as he became discontented with a lack of consideration with the growth of human potential by Freud and his followers, and during the 20's and 30's began to develop his own theory and methods. Only in the 50's and 60's was his work recognized outside of Italy.

Frederick (Fritz) Perls (1893-1970)

  Perls was a Freudian trained psychoanalyst, the founder of Gestalt therapy, and a charismatic figure. Born in Berlin, he received his M.D. from Frederich Wilhelm University, and then received a psychoanalytic training with Wilhelm Reich as his analyst. He met many of the key founders of Gestalt psychology (Kohler, Wertheimer, Lewin) and worked as Kurt Goldstein's assistant. He went to South Africa in 1934, where he set up the Institute of Psychoanalysis, and met Jan Smuts, the inventor of the term "holism". Moving to the USA in 1946, with his wife he set up the New York Institute of Gestalt Therapy in 1952.

Viktor Frankl (1905-1997)

  Frankl saw that each person's suffering is unique, and opportunity for growth lies in the way the person bears their suffering. Logotherapy is an attempt to implement that insight in a therapeutic context. Frankl had been strongly influenced by the existential philosophers, Heidegger and Jaspers, and began to develop a philosophy of his own. As the titles of his many popular books suggest, Logotherapy is concerned basically with meaning, the will to meaning, the unheard cry for meaning.

And a few others

Gordon Allport (1897–1967)

You mentioned Gordon Allport in your question and yet he is not mentioned by Dr. David R. Hiles, or Reeves above, which is interesting because it is argued that the term "humanistic psychology" was first coined by Gordon Allport in 1930 (DeCarvalho, 1991).

(Allport, 1930) under the subheading of 'A new Science Needed' said:

  My points, I fear, have been arbitrarily chosen and rather dogmatically presented.  In no other way, however, is it possible to illustrate in a short time the thesis of this paper, namely that a deliberate formulation of a science of personality is not only a necessary but an altogether possible task.  It is mere laziness to insist that knowing people is an art, and therewith to dismiss the subject.  If knowing people is an art, it seems to be an art which, like medicine, can be formulated and communicated, and which can and should be included within a new and broader type of humanistic psychology (p.127, italics added)

DeCarvalho states that you can find similar statements in all of Allport's major works and particularly in the 1960s.

  Ignorance of Allport's use of the term humanistic psychology is symbolic of a larger ignorance of Allport's contribution to the humanistic current in American psychology: This omission occurs not only in the texts of the history and systems of psychology, but unfortunately also among humanistic psychologists themselves.....Allport was a well-known personality theorist and perhaps the most prestigious thinker of the early and mid-20th century psychological world who championed the humanistic movement in psychology in the earliest stages. (DeCarvalho, 1991)

References

Allport, G. W. (1930). Some guiding principles in understanding personality. The family, 11(4), 124-128.DOI: 10.1177/104438943001100407Free PDF: http://journals.sagepub.com/doi/pdf/10.1177/104438943001100407

Counselling Directory (n.d.) Humanistic Therapies. [Online]
Available at: http://www.counselling-directory.org.uk/humanistic.html
[Accessed 16 February 2017].

DeCarvalho, R. J. (1991). Gordon Allport and humanistic psychology. Journal of Humanistic Psychology, 31(3), 8-13.DOI: 10.1177/0022167891313002

Maslow, A. (1968). Toward a Psychology of Being. New York: Van Nostrand.

Reeves, A. (2013). An Introduction to Counselling and Psychotherapy: From Theory to Practice. London: SAGE Publications Ltd.

Short, F. & Thomas, P. (2015) Core Approaches in Counselling and Psychotherapy. Hove: Routledge.


How to interpret neuron spiking models one comes across in literature? Background

I'm in high school currently conducting research (obviously it is relatively rudimentary compared to what is being done in the labs, etc.) in computational neuroscience.

I'm dealing with multiple datasets each containing time series data for a majority of neurons in C. Elegans (the dataset is the one used in Saul Kato's Global Brain Dynamics Embed the Motor Command Sequence of Caenorhabditis elegans).

I'm looking to do a pairwise comparison of each neuron in every dataset; if $N_{ij}$ is the $j^{th}$ neuron in the $i^{th}$ dataset, then I will do a pairwise comparison of all neurons in the $j^{th}$ column.

Question

I'm going through this paper which proposes a method of comparing time series data across neurons. The paper uses this spiking model:

I'm wondering how neuroscientists approach such models they read about in literature; how they dissect it mathematically, what crosses their mind when they look at these models, etc. and where I can go to gain a rigorous foundation to truly and intuitively understand the models I read about in the future.

Read dayan and abbot "theoretical neuroscience"
Learn differential equations
Know the relationship between voltage, current, resistance and conductance
Differential equations is absolutely essential though. you don't need to learn to solve them (the computer will do that for you), you just need to learn to know what they mean.
How do researchers translate observations of nature into symbolic, mathematical approximations/models of these phenomena? By gaining intuition of how the model components relate to empirical observations. it is relatively rare that someone comes up with a new model from scratch. most of the time people retool or remix previous models.


Affective Neuroscience Personality Scales I wonder if anybody could give some details about Affective Neuroscience Personality Scales. I tried to access 'The Affective Neuroscience Personality Scales: Normative Data and Implications' by Kenneth L. Davis, Jaak Panksepp, Larry Normansell, but I have no access.

That paper is kinda old and as you point out it is paywalled. Try this free paper instead.
A brief form of the affective neuroscience personality scales.

The Affective Neuroscience Personality Scales (ANPS) were developed to measure behavioral traits related to 6 affective neurobiological systems (play, seek, care, fear, anger, and sadness). However, the ANPS has a number of problems, including an ill-defined factor structure, overly long scales, and items that are poorly worded, ambiguous, and of questionable content validity. To address these issues, we constructed an improved short form of the ANPS--the Brief ANPS (BANPS). Three studies demonstrated that the 33-item BANPS has a clear and coherent factor structure, relatively high reliabilities (for short scales), and theoretically meaningful correlations with a wide range of external criteria, supporting its convergent and discriminant validity. Unlike typical short-form scales, the BANPS improves upon the psychometric properties of the long form, and we recommend its use in all research contexts.

This is the only other paper I have the ability to cite about ANPS:
The brain's emotional foundations of human personality and the Affective Neuroscience Personality Scales

The anatomical, neurochemical, and functional homologies of subcortical emotional networks strongly indicate underlying evolutionary continuities in affective principles in all mammalian brains (Panksepp and Biven, 2011). Since it is widely believed that individual's emotional inclinations (temperaments) are foundational for human personality development, the goal of the following work was to try to ground personality assessment on the affective circuits that all mammals share. But before we summarize work with the Affective Neuroscience Personality Scales (ANPS), we briefly note historical antecedents of this way of thinking about human personality.
We sustained the capitalization convention in our attempt (i.e., the ANPS) to translate anoetic (without knowledge) emotional experiences to noetic (knowledge linked) and autonoetic (thought linked), language-based evaluations of the potential influences of primal affects in the personality structures of human minds. However, rather than RAGE and PANIC/GRIEF, we decided to use the terms ANGER and SADNESS in this paper and in our construction of the Affective Neuroscience Personality Scales (ANPS), since those are labels that are generally more understandable for most individuals. Still, the theoretical implication is that these systems are critically important for the various feelings highlighted by these scientific terms – e.g., the ANGER system energizes states commonly labeled as ‘irritability’ and ‘anger’.
There are several principles basic to understanding these seven brain systems: (1) These emotion systems are subcortical networks and lower brain regions have evolutionary primacy in generating these basic emotions and their affects, while learning and higher brain functions can be deemed to be secondary and tertiary processes. (2) To the best of our knowledge, these emotion systems, situated in ancient brain regions, are largely homologous in all mammals. (3) These basic emotions also have similar chemistries in all mammals. (4) These brain systems generate instinctual behavioral responses that are closely linked to the raw, primal affects that accompany those responses. (5) The integrity of these seven systems is demonstrated by the ability to elicit coherent specific emotional responses and/or the associated affects with localized brain stimulation – as evaluated by the capacity of the subcortical arousals to mediate ‘reward’ and ‘punishment’ functions that control learning. (6) Lastly, these systems remain relatively unscathed in animals whose neocortices were surgically removed in early development (see Panksepp, 1998).
In summary, emotional responses from each of the primary process emotions can be activated by localized subcortical ESB or chemical brain stimulation. That decortication of young animals generally leaves the expression of these emotions intact (Deyo et al., 1990 and Panksepp et al., 1994), further reinforces the subcortical nature of these emotion systems. Also, each instinctual emotional system engenders affective valence since animals terminate the stimulation of ANGER, FEAR, and SADNESS, while actively working to obtain SEEKING, LUST, CARE, and PLAY system arousals (Panksepp, 2005). However, there are reasons to believe the SEEKING system is foundational for aspects of all of the other primal emotions (e.g., during FEAR intensification, the shift from freezing to flight may be due to recruitment of SEEKING related dopaminergic psychomotor drive).
Based on our first study using these scales, reliabilities for the ANPS scales, computed as Cronbach's alpha, were reported ranging from .65 to .86 with the PLAY and SEEK scales below .70 and the FEAR, ANGER, and Spirituality scales above .80 (Davis et al., 2003). Multiple data sets using the revised ANPS 2.4, have shown all reliabilities now over .70 (unpublished data).
Contrasting self-rating data for ANPS and FFM scales, as seen in Table 1, revealed that each of the ANPS scales except Spirituality correlated strongly with at least one of the FFM scales as follows: (1) SEEK with Openness to Experience (r = .47), (2) PLAY with Extraversion (r = .46), (3) CARE with Agreeableness (r = .50), (4) FEAR with Emotional Stability (r = −.75), (5) SADNESS with Emotional Stability (r = −.68), and (6) ANGER with Emotional Stability (r = −.65) as well as with Agreeableness (r = −.48) (Davis et al., 2003). The data supported strong relationships between primary emotions and the most widely accepted model of human personality, which was consistent with the hypothesis that these six brain emotion systems form a foundation for the adult five-factor personality model.


What's the difference between executive functions and cognitive control? I suspect that the difference between these terms may vary from researcher to researcher, since the wikipedia page treats them as synonymous. What's the difference between executive functioning and cognitive control? Is cognitive control a type of executive function?

You are right to suspect that cognitive control and executive function are essentially interchangeable, at least for most purposes. Among researchers in the area, I would say there is a slight difference, however.

Cognitive control refers to the more abstract concept and affords researchers more degrees of freedom in defining what that means operationally speaking. Here is a fairly representative example of its use, from Botvinick et al. (2001), found on a quick Scholar search:

  A remarkable feature of the human cognitive system is its ability to configure itself for the performance of specific tasks through appropriate adjustments in perceptual selection, response biasing and the on-line maintenance of contextual information. The processes behind such adaptability, referred to collectively as cognitive control ...

Executive function, meanwhile, tends to either depend directly or conceptually on the seminal paper by Miyake et al. (2000), which more explicitly models this sort of control in terms of shifting, updating and inhibition functions. This is an extremely influential and productive model, and at least within the context of working memory research, I would say it sees more use than the more conceptual 'cognitive control'.

References

Botvinick, M. M., Braver, T. S., Barch, D. M., Carter, C. S., & Cohen, J. D. (2001). Conflict monitoring and cognitive control. Psychological review, 108(3), 624.
Miyake, A., Friedman, N. P., Emerson, M. J., Witzki, A. H., Howerter, A., & Wager, T. D. (2000). The unity and diversity of executive functions and their contributions to complex “frontal lobe” tasks: A latent variable analysis. Cognitive psychology, 41(1), 49-100.


How did Shaver (1970) manipulate similarity in the defensive attribution study? Shaver (1970) had two independent variables, severity of the accident outcome (severity) and similarity of the subjects to the transgressor.

Severity was manipulated by giving subjects in different conditions different scenarios:

mild outcome = the boy had the metal splinter in his wrist
severe outcome = the boy had a metal splinter in his eye

How did Shaver “manipulate” the IV similarity (similar/dissimilar)?

References

Shaver, K.G. (1970). Defensive attribution: Effects of severity and relevance on the responsibility assigned for an accident In: Journal of Personality and Social Psychology, 14(2): pp 101-113.
DOI: 10.1037/h0028777

This article has several experiments included in it. These have different operational definitions of variables, and specifically differ in their definitions of "similarity". I'll assume you are talking about Experiment 3 where the hypothetical child is injured. From the end of Experiment 2 (p. 108, c. 2, first full paragraph):

  ... a third experiment was conducted in which perceived personal similarity was one of the dependent variables ... Thus, only severity of consequences was
  actually manipulated.

So for this situation (Experiment 3), similarity is actually treated as an outcome and is not manipulated.


Why do humans like being touched? Why do people like to be touched so much, why would it make sense from a evolutionary perspective.

I know people enjoy hugs and company of opposite sex, but even people from the same sex hug and touch each other.

I wonder how this behavior could have evolved. Was it the struggle to keep warm that drawn people physically together? Does it all have to do with mating?

Maybe there just isn't enough data to specify how this behavior started out?

Of all the senses, touch is the one that most connects a person to the external environment. When two people touch each other (a handshake, a hug, a kiss, etc.) a connection/bond is made. This bonding is deeply involved with social development and emotional interaction.

Interpersonal relationships are essential for social interactions. It is important to known where the boundaries are in your culture, so that personal space is respected. This varies widely between cultures and persons.


Is Paul's Churchland claim about qualia supported by science? Knowledge argument:

  Mary is a brilliant scientist who is, for whatever reason, forced to investigate the world from a black and white room via a black and white television monitor. She specializes in the neurophysiology of vision and acquires, let us suppose, all the physical information there is to obtain about what goes on when we see ripe tomatoes, or the sky, and use terms like "red", "blue", and so on. She discovers, for example, just which wavelength combinations from the sky stimulate the retina, and exactly how this produces via the central nervous system the contraction of the vocal cords and expulsion of air from the lungs that results in the uttering of the sentence "The sky is blue". [...] What will happen when Mary is released from her black and white room or is given a color television monitor? Will she learn anything or not?

Paul's Chuchland answer is:

  According to Paul Churchland, Mary might be considered to be like a feral child. Feral children have suffered extreme isolation during childhood. Technically when Mary leaves the room, she would not have the ability to see or know what the color red is. A brain has to learn and develop how to see colors. Patterns need to form in the V4 section of the visual cortex. These patterns are formed from exposure to wavelengths of light. This exposure is needed during the early stages of brain development. In Mary's case, the identifications and categorizations of color will only be in respect to representations of black and white.

But can't I really see new color if I never experienced some mixture of wavelengths prior? I thought that the person who saw only 90% of spectrum for the whole life still would gain new experience when seeing something from remaining 10%.

I know cone cells are responsible for color perception. They are located on retina of eyes. Most people have three of them, but there can be more or less. Signals from them travel to parvocellular cells and to koniocellular cells. It's not clear how color is processed there, as far as I am aware. Then signals travel to visual cortex from there. And V1 is said to be the most influential part of visual cortex. But I am not sure how V4 is responsible for color perception.

Is there scientific support for his claim? Or instead, is there scientific support for the opposite?

Read further down to

  The neural basis of qualia

  V.S. Ramachandran and Edward Hubbard of the Center for Brain and Cognition at UCSD argue that Mary might do one of three things upon seeing a red apple for the first time:

  Mary says she sees nothing but gray.
  She has the "Wow!" response from subjectively experiencing the color for the first time.
  She experiences a form of blindsight for color, in which she reports seeing no difference between a red apple and an apple painted gray, but when asked to point to the red apple, she correctly does.

  They explain further: "Which of these three possible outcomes will actually occur? We believe we've learned the answer from a colorblind synesthete subject. Much like the theoretical Mary, our colorblind synesthete volunteer cannot see certain hues, because of deficient color receptors. However, when he looks at numbers, his synesthesia enables him to experience colors in his mind that he has never seen in the real world. He calls these "Martian colors." The fact that color cells (and corresponding colors) can activate in his brain helps us answer the philosophical question: we suggest that the same thing will happen to Mary."[21]

So it is possible to see in your mind colors you've never seen in reality, due to defective receptors. But it's possible that synesthesia in this subject caused some pathways to form that do not exist in someone who never experienced any color even even due to "fake" inputs like synesthesia.

One fairly recent (2012) fMRI study on a late-blind synaesthete found that

  The colour area hOC4v was engaged when the synaesthetic experience included colour. These results confirm the continued recruitment of visual colour cortex in this late-blind synaesthetes.

So it's technologically possible to determine/confirm when color "perception" in the brain is occurring in the blind. All it would take now is a subject for whom the order of events is reversed (born blind, but acquired/induced synesthesia.) The last paper notes however that.

  It is known that differences in the functional
  neuroanatomy of sighted and early-blind subjects reflect predominantly early recruitment of visual cortical areas for
  tactile [...] and auditory stimulation [...], and during
  verbal [...], and memory processing
  [...]. However, in late-blind individuals, visual cortical areas seem to retain some aspects of their
  original specificity. For instance, tactile perception of motion and faces activates visual cortical areas previously involved in
  analysis of equivalent visual stimuli [...]. And in a late blind synaesthete (the subject of the
  present report), both striate and extrastriate visual areas appeared to be engaged in the synaesthetic perception of coloured
  and spatially located concurrents [...].

So it's not a foregone conclusion that the early- or congenitally-blind could still/even experience synaesthetic color.

One 2018 study (Dell'Erba et al.) on the subjective experiences of a congenitally-blind man on psychedelic drugs reported that these include "synesthetic hallucinations", but of the tactile kind, and the complete absence of visual hallucinations, in line with their (previously reported) absence from the congenitally blind in general.

A Harlow-type experiment in monkeys (for the development of color vision in a black-and-white environment) might barely clear ethics boards nowadays. However, monkeys with natural [partial] color blindness can get the "full version" though gene therapy, suggesting that at least the color machinery in the brain, if developed for two colors/sensors, can quickly accommodate three thereafter. This result however (besides the coolness of gene therapy) isn't terribly surprising on a phenomenological level, given the reports of synesthesic "martian colors" in the color blind humans. (More interestingly, giving mice three-colored vision doesn't work as well.)

Much more interesting for our discussion is achromatopsia and its (genetic) treatments:

  Achromatopsia is a rare (1 in 30,000 to 80,000) congenital visual condition characterized by diminished or absent cone photoreceptor function. Patients have severely reduced visual acuity (~20/200), nystagmus and photophobia. Causative autosomal recessive mutations affect genes of the cone phototransduction cascade, CNGA3, CNGB3, GNAT2, PDE6H, PDE6C, [...] or the transcription factor ATF6. A subset of patients have unidentified causative mutations. Patients typically show complete cone function loss, as shown by absent cone-isolating electroretinogram (ERG) recordings. An incomplete phenotype occurs more rarely, but is not clearly correlated to the underlying mutation. Achromatopsia affects all three classes of photoreceptor and hence, by definition, relates to genes that are expressed in all cone subtypes, as listed above. Conversely, blue monochromatism, tritanopia, and red-green color blindness (deuteranopia and protanopia) are caused by mutations in genes specific to certain subtypes of cone photoreceptors; an important difference to achromatopsia. [...]

  A well reported achromatopsia population lived on the South Pacific island of Pingelap. A genetic bottleneck following Typhoon Lengkeki in 1775 created a founder effect and over 10 percent of the island population had complete achromatopsia. The story is notably recorded in The Island of the Colorblind by the neurologist and author, Oliver Sacks. [...]

  phase I clinical trials to treat achromatopsia using an AAV vector to deliver CNGA3 have already started in Germany (NCT02610582), CNGA3 in the USA and Israel (NCT02935517), CNGB3 in the USA (NCT02599922), and CNGB3 in the UK (NCT03001310) [...]

These are in the wake of partially successful animal knockout models & treatments thereof.

  Carvalho et al. (2011) explored the therapeutic age window for gene therapy in achromatopsia. A mouse model caused by a premature stop codon was rescued with human CNGB3 transgene packaged in an AAV8 capsid. The use of a cone arrestin promoter fragment resulted in universal expression in all cone subpopulations, an alternative solution to the use of the ubiquitous CBA promoter. The subretinal vector rescued retinal function, as tested by ERG, at a range of ages, but again there were poor visual responses in mice treated at later ages. This confirmed that there is an optimal therapeutic window at a younger age. The limited benefit at later ages may be a result of slow retinal degeneration in this model or amblyopia. Cone outer segment abnormalities have also been noted in achromatopsia animal models and it has been shown that regenerating the outer segments with intravitreal ciliary neurotrophic factor just before achromatopsia gene therapy may improve the responses significantly in older Cngb3 deficient mice.

The treatments were also successful for serendipitous "models" found in some sheep (age of the animals is not discussed in this latter context, alas):

  Two serendipitous discoveries of day blindness in unrelated Awassi sheep flocks in Israel yielded two new large-animal models of Cnga3 achromatopsia. Both models—a premature stop codon and a missense mutation—were rescued using the same human PR2.1-CNGA3 vector described by Komaromy et al. (2010). As expected, photopic ERG was restored. Treated animals were also able to use the restored cone function to navigate a maze in photopic conditions. A mouse Cnga3 transgene also provided a similar rescue effect.

The authors of this review generally conclude/speculate that

  The implications for human achromatopsia gene therapy are that the treatment will most likely need to be applied in early childhood to be maximally effective. [...]

  The [four human] trials are designed to initially test the safety profile in adult patients, but three of the trials plan to include patients as young as 6 years in later groups. By comparing older and younger patients, the trials will examine differences in integrated functional cone rescue between age groups. If the pattern observed in the animal trials holds true, there may be a difference in benefit due to patient age at time of treatment. Such a difference may arise from reorganization of cortical pathways or foveal hypoplasia.

  In the one other therapeutic trial registered for achromatopsia (ClinicalTrials.gov number, NCT01648452), six CNGB3 achromatopsia patients received intraocular implants that released Ciliary Neurotrophic Factor (CNTF). CNTF provides neuroprotection to rod and cone photoreceptors in degenerative retinal disease. Concurrent treatment with intravitreal CNTF in a canine model of CNGB3 achromatopsia potentiated gene therapy rescue. CNTF improved ERG rescue in older animals, overcoming a notable inability of gene therapy alone to benefit most dogs over 1 year of age. Limited evidence suggested that CNTF pre-treatment de-differentiated the cone photoreceptors by elongating the outer segments to facilitate CNGA3/B3 tetrameric protein assembly. As mentioned above, in the CNTF only trial, no functional improvement in cone function occurred. There are no current plans to include CNTF pre-treatment in any of the registered human gene therapy trials. This discussion may be reignited if the early trials show difficulty in rescuing cone function in older patients.

So the aforementioned (ongoing as of mid-2017) human trials should have interesting things to say about human color vision development in the absence of all three color "sensors"...


Has there been any research on the visual uniqueness (in terms of brain activity) of numerals from 0 to 9? I need to carry out EEG experiments with stimuli being images of 5 digits between 0 and 9. In order to select these 5 digits, I wanted to know if there has been any research work that measures relative brain activity while observing numerals.

I have been able to find similar work for text (orthographic coding), but not for visual processing. Please let me know if you know of any such work.

Thanks in advance!

Not sure, but I think you'd find it interesting that there are some humans out there who do not have an intuitive sense of any number past two. For example, people who are part of hunter gatherer tribes who, for example, only need to know that they have a lot of berries, not that they have exactly 7 or exactly 65; for their lifestyle, there is no need for counting. Their numbers are "1", "2", and "more than 2", and their language lacks the capability to express any other numerical idea.

Presumably this has an effect on the physiology of their brain. I'm pointing this out because maybe it suggests that something as specific as the numerical digits 0-9, which are represented with different symbols even across cultures that have all 10 digits, are too specific to elicit any sort of measurable difference in brain activity while reading one compared to the other. And that's the reason no studies have been done on them. Am totally unsure of this.


Why do long range axons in mammals travel in white matter tracts? I am curious to know as to why long range, myelinated axons prefer to convene and form white matter tracts, rather than simply reach its target in an arbitrary fashion. Is there some kind of evolutionary advantage to this phenomena? Or is this an ongoing research question?

Wen & Chklovskii (2005) looked at exactly this question through a simulation study. They assumed that the segregation of white and gray matter was the the result of evolutionary pressure to maximize some aspect of connectivity. They tested the idea that simultaneously maximizing interconnectivity (neurons should be able to connect to all other neurons without too many intermediate steps) and minimizing conduction delay (time required for a signal to travel from one neuron to another) would result in the segregation of gray and white matter.

Through computational simulation, they were able to determine that these simultaneous pressure were sufficient to drive the white/gray matter divide. Part of what they were able to show is that, under some simple geometric assumptions, a mixed (homogeneous) design that had white matter interspersed with gray matter led to much higher conduction delays than a segregated design. The basic reason is that when white matter is mixed in with the gray matter, the short-range connections between nearby neurons in gray matter are longer to account for the interference of the white matter tracts.

Wen, Q., and Chklovskii, D.B. (2005). Segregation of the brain into gray and white matter: A design minimizing conduction delays. PLoS Comput Biol, 1(7): e78. doi:10.1371/journal.pcbi.0010078


What is the set of cards used in the Wisconsin/Berg Card Sorting task? I'm a little confused about what cards are included in the Wisconsin card sorting task. According to PEBL there are two sets of cards available for the task, one set of 64 cards and one set of 128 cards. I think I've figured out what the 64 card deck is given that there are four different number, four different colours and four different shapes. Consequently, 4*4*4=64. However, what is contained in the 128 card deck?

The 64 card version is just a shorter version, according to (Greve, 2001). Instead of running 128 total trials, there are only 64. The original test was developed and, crucially, normed for 128 trials. However, this version takes a long time to administer, and clinicians were interested in a shorter version. It was found that cutting the number of trials in half worked reasonably well.

So the short answer seems to be that the decks are the same.