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

Question

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?

Answer 1

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:

1. Mary says she sees nothing but gray.
2. She has the "Wow!" response from subjectively experiencing the color for the first time.
3. 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"...