One way I could be wrong is if the neural circuitry for trichromacy exists but is dormant in such individuals.
If they have grown up without proper trichromatic neural signals flowing from the retina to the LGN into V1, then V1 will have already developed a set of low level gabor features that are bichromatic. To actually see in color, the visual systems of these patients will need to do some relearning.
Based on other known plasticity/rewiring experiments, it seems fairly reasonable that this type of rewiring will occur automatically as a result of new explained spike signal components flowing into V1.
As a reference example, MIT did these famous experiments way back in the day where students put on these special goggles that flip vision completely (vertically I believe). Apparently the patients reported that at first everything was upside down, confusing, and even nausating. However after some period of time (a week or two?) there is a sudden aha moment and their vision ‘flips’ and they can see normally—with the goggles on. Removing the goggles then results in a similar process, but with faster relearning.
All of this can be explained in an ANN type model with continuous incremental online (gradient descent style) learning dynamics. The aha moments even correspond to the rather sudden phase transitions seen in the evolution of ANN weights.
I have no doubt that rewiring like that can and will happen. But then there’s the question of why introducing new photoreceptors is special in this regard. And if this type of stimulus can’t be produced by other means (like seeing the world through a special camera setup, like I mentioned), and, if so, if such other means could in fact produce novel color qualia. After all, all we’re doing is making some modifications to the most superficial part of the visual neural system.
But then there’s the question of why introducing new photoreceptors is special in this regard.
Because introducing new signals from new photoceptors changes the network dynamics and leads to new concept learning.
And if this type of stimulus can’t be produced by other means (like seeing the world through a special camera setup, like I mentioned), and, if so, if such other means could in fact produce novel color qualia.
From the information you provided, I suspect that the deuteranomaly case is functionally similar or equivalent to the bichromatic case. What really matters is the actual connectivity structure of the gabor filters in V1.
if so, if such other means could in fact produce novel color qualia.
Well, theoretically you could add even more chromatic signals—for infrared say—and if V1 rewires to include those signals, then the patient would report a new infrared color qualia, of a type no human had experienced.
On a related note, there is a wierd experiment involving a device that encodes images onto the surface of the tongue, allowing blind patients to ‘see’ the output of a camera through their tongue. That could be considered a new ‘qualia’, as the resulting visual pathway is undoubtedly quite different than normal.
If they have grown up without proper trichromatic neural signals flowing from the retina to the LGN into V1, then V1 will have already developed a set of low level gabor features that are bichromatic. To actually see in color, the visual systems of these patients will need to do some relearning.
Based on other known plasticity/rewiring experiments, it seems fairly reasonable that this type of rewiring will occur automatically as a result of new explained spike signal components flowing into V1.
As a reference example, MIT did these famous experiments way back in the day where students put on these special goggles that flip vision completely (vertically I believe). Apparently the patients reported that at first everything was upside down, confusing, and even nausating. However after some period of time (a week or two?) there is a sudden aha moment and their vision ‘flips’ and they can see normally—with the goggles on. Removing the goggles then results in a similar process, but with faster relearning.
All of this can be explained in an ANN type model with continuous incremental online (gradient descent style) learning dynamics. The aha moments even correspond to the rather sudden phase transitions seen in the evolution of ANN weights.
I have no doubt that rewiring like that can and will happen. But then there’s the question of why introducing new photoreceptors is special in this regard. And if this type of stimulus can’t be produced by other means (like seeing the world through a special camera setup, like I mentioned), and, if so, if such other means could in fact produce novel color qualia. After all, all we’re doing is making some modifications to the most superficial part of the visual neural system.
Because introducing new signals from new photoceptors changes the network dynamics and leads to new concept learning.
From the information you provided, I suspect that the deuteranomaly case is functionally similar or equivalent to the bichromatic case. What really matters is the actual connectivity structure of the gabor filters in V1.
Well, theoretically you could add even more chromatic signals—for infrared say—and if V1 rewires to include those signals, then the patient would report a new infrared color qualia, of a type no human had experienced.
On a related note, there is a wierd experiment involving a device that encodes images onto the surface of the tongue, allowing blind patients to ‘see’ the output of a camera through their tongue. That could be considered a new ‘qualia’, as the resulting visual pathway is undoubtedly quite different than normal.