Abnormal retino‐geniculate and geniculo‐cortical pathways in several genetically distinct color phases of the mink (Mustela vison)

Abstract

Several genetically distinct color phases of mink, which all show an abnormal reduction of pigment in the retinal pigment epithelium and which also show abnormalities of the retinofugal pathways, have been studied. Autoradiographic methods have been used to demonstrate the retino‐geniculate pathways, and retrograde degeneration or the retrograde transport of horseradish peroxidase has been used for the geniculo‐cortical pathways.The retino‐geniculate abnormality is mild in some of the color phases and extremely severe in others, but within any one color phase the variability is relatively low. Although the severity of the abnormality varies between color phases, a rather specific pattern of abnormal geniculate innervation is recognizable for mink in general and this is distinct from that found in Siamese cats. In the abnormal mink the size of geniculate lamina A1 is reduced and there is an abnormal crossed input going to the intermediate sectors of this reduced layer. Layer C1 also receives an abnormal crossed input, but this is more variable than that going to A1 and there appears to be little correspondence, retinotopically, between the normal inputs to layers A1 and C1. In some of the abnormal mink there are interruptions within the cytoarchitectonically definable layer A1, and opposite these gaps reduplications of layer A are commonly seen, as though there is an intrinsic geniculate mechanism for generating the characteristic multilaminar geniculate structure. However, there are also numerous examples of fusions between layers receiving afferents from the same eye, and these demonstrate that the development of geniculate lamination must also be under the influence of the retinal inputs.The geniculo‐cortical pathway shows a normal topography in most of the mink. Abnormal geniculo‐cortical projections, comparable to the “Boston” pattern of Siamese cats are extremely rare, and their occurrence could not be correlated with the severity of the retino‐geniculate abnormality or with the laminar pattern in the lateral geniculate nucleus. We suggest that the development of one or the other pattern of geniculo‐cortical projection may depend upon the relative timing of the two mechanisms that produce the geniculate lamination.