Volume and neuron number of the lateral geniculate nucleus in schizophrenia and mood disorders.

Subjects with schizophrenia show deficits in visual perception that suggest changes predominantly in the magnocellular pathway and/or the dorsal visual stream important for visiospatial perception. We previously found a substantial 25% reduction in neuron number of the primary visual cortex (Brodmann's area 17, BA17) in postmortem tissue from subjects with schizophrenia. Also, many studies have found reduced volume and neuron number of the pulvinar--the large thalamic association nucleus involved in higher-order visual processing. Here, we investigate if the lateral geniculate nucleus (LGN), the visual relay nucleus of the thalamus, has structural changes in schizophrenia. We used stereological methods based on unbiased principles of sampling (Cavalieri's principle and the optical fractionator) to estimate the total volume and neuron number of the magno- and parovocellular parts of the left LGN in postmortem brains from nine subjects with schizophrenia, seven matched normal comparison subjects and 13 subjects with mood disorders. No significant schizophrenia-related structural differences in volume or neuron number of the left LGN or its major subregions were found, but we did observe a significantly increased total volume of the LGN, and of the parvocellular lamina and interlaminar regions, in the mood group. These findings do not support the hypothesis that subjects with schizophrenia have structural changes in the LGN. Therefore, our previous observation of a schizophrenia-related reduction of the primary visual cortex is probably not secondary to a reduction in the LGN.

Pax6 regulates regional development and neuronal migration in the cerebral cortex.

Mutations in the Pax6 gene disrupt telencephalic development, resulting in a thin cortical plate, expansion of proliferative layers, and the absence of the olfactory bulb. The primary defect in the neuronal cell population of the developing cerebral cortex was analysed by using mouse chimeras containing a mixture of wild-type and Pax6-deficient cells. The chimeric analysis shows that Pax6 influences cellular activity throughout corticogenesis. At early stages, Pax6-deficient and wildtype cells segregate into exclusive patches, indicating an inability of different cell genotypes to interact. At later stages, cells are sorted further based on telencephalic domains. Pax6-deficient cells are specifically reduced in the mediocaudal domain of the dorsal telencephalon, indicating a role in regionalization. In addition, Pax6 regulates the process of radial migration of neuronal precursors. Loss of Pax6 particularly affects movement of neuronal precursors at the subventricular zone/intermediate zone boundary at a transitional migratory phase essential for entry into the intermediate zone. We suggest that the primary role of Pax6 is the continual regulation of cell surface properties responsible for both cellular identity and radial migration, defects of which cause regional cell sorting and abnormalities of migration in chimeras.