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Observations on the organization of the visual cortex in the reeler mouse

1981; Wiley; Volume: 201; Issue: 4 Linguagem: Inglês

10.1002/cne.902010407

1096-9861

Ursula C. Dräger,

Neuroscience and Neuropharmacology Research

Abstract The developmental abnormality caused by the autosomal recessive mutation reeler leads to a systematic inversion in the depth distribution of morphologically defined cell classes in the cortex and to an abnormal course taken by thalamocortical projections (Caviness, '77). The course of the geniculocortical projections was visualized in reeler through transneuronal autoradiography. After traveling under the pial surface, the fibers terminate in a slightly patchy manner at intermediate levels of the primary visual cortex. As in the normal mouse, there is a weaker projection to the lateral part of area 17 ipsilateral to the injection. The retinal ganglion cells giving rise to the ipsilateral projection in reeler were labeled with horseradish peroxidase and were found to be located at normal positions in the retina. The functional competence of the primary visual cortex in reeler was studied by recording the response properties of single cells. In most respects the reeler cortex appeared remarkably normal: the cortical topography of the visual‐field representations was normal overall, all receptive field types seen in the normal mouse were present, and cells within the binocular region received normally convergent input from the two eyes. The reeler differed from normal in having a greater number of poorly responding cells and a lower fraction of cells with oriented receptive fields. The tendency for oriented cells to occur preferentially in upper cortical layers in the normal mouse was not present in reeler. These results imply that the cells in the reeler cortex are connected in a largely normal manner despite the gross malformation. Thus it appears that the specificity of intercellular connections, in reeler and in normal cortex, does not depend crucially upon the position of the cells in the cortex.