manhattan, are you sure this shouldn’t be in GD? 
Anyway, I don’t have an opinion as of yet, but I thought you might find the following information about cats interesting and relevant to the above article. This information has been around for quite a while, as the book I’m quoting from was published in 1991:
From Feline Husbandry: Diseases and Management in the Multiple-Cat Environment, by Niels C. Pedersen, DVM, PhD, published by American Veterinary Publications. pp 86 - 87
"Albino mammals completely lack melanin pigment; hence, their eyes are pink or red and the coat white. They also have a misrouting of the visual pathway from the retina to the brain.(My bold) the anomaly has been detected in albinos of all species so far examined, including Syrian hamsters, guinea pigs, rabbits, mice, rats, ferrets, mink and one species of monkey. The visual pathway is affected in cats carrying either the albino (c) or Siamese (c(s)) allele, but not the Burmese (c(b)) allele.
The ganglion axons from the retinal cells of the eye normally travel to the lateral geniculate nucleus of the thalamus. This nucleus is sited in each side of the brain. Each eye contributes fibers to defined layers of the lateral geniculate nuclei. A disproportionate number of the fibers in the Siamese cat . . . crosses to the lateral geniculate nucleus on the side opposite to the eye. The lateral geniculate nuclei are incorrectly innervated in reverse order. the cat’s brain probably does not receive a distorted picture, however.
Elegant experiments suggest the the visual field is compensated by either of 2 methods. The most direct is apparent suppression of the abnormal information when it reaches the visual cortex (the “mid-western pattern”). The other compensation method involves rearrangement of information inputs to recreate a normal visual field (the “Boston pattern”). The 2 methods of compensation may not be absolute, but rather part of a continuum. The method of compensation may depend upon the extent of the erroneous crossover of ganglions. Misrouting is present from the earliest prenatal stages of development of the ganglion pathway and arises at the optic chiasm. Misrouting is present from the earliest prenatal stages of development of the ganglion pathway and arises at the optic chiasm. Misrouting may interfere with normal binocular depth perception and is responsible for the convergent squint to which Siamese are particularly prone.
The Siamese allele . . . falls short of complete albinism, but the complete albino alele . . . has recently been recognized. Examination of the visual pathway in albinos reveals misrouting to be much greater than in Siamese. A much higher proportion of the ganglion axons crosses over to the opposite lateral geniculate nucleus. As a consequence, organization of the visual field in the cortex differs from that observed for Siamese. The albino allele is completely recessive to full color (C) as regards eye and coat color, but not for misrouting of ganglion axons. Heterozygous Cc albinos or Siamese have similar misrouting, but less extreme." (Ellipses used in place of some difficult-to-reproduce genetic notation.)
In other words, mammals that are albino, albino series mutations, or who carry a recessive albino/albino series gene have differently wired visual pathways - but still apparently see and function quite well. Hmm, some of this info might have inspired the ferret re-wiring experiment.
Brains are certainly versatile organs.
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