The expression of cadherin-8 was mapped by in situ hybridization in the embryonic and postnatal mouse central nervous system (CNS). From embryonic day 18 (E18) to postnatal day 6 (P6), cadherin-8 expression is restricted to a subset of developing brain nuclei and cortical areas in all major subdivisions of the CNS. The anlagen of some of the cadherin-8-positive structures also express this molecule at earlier developmental stages (E12.5-E16). The cadherin-8-positive neuroanatomical structures are parts of several functional systems in the brain. In the limbic system, cadherin-8-positive regions are found in the septal region, habenular nuclei, amygdala, interpeduncular nucleus, raphe nuclei, and hippocampus. Cerebral cortex shows expression in several limbic areas at P6. In the basal ganglia and related nuclei, cadherin-8 is expressed by parts of the striatum, globus pallidus, substantia nigra, entopeduncular nucleus, subthalamic nucleus, zona incerta, and pedunculopontine nuclei. A third group of cadherin-8-positive gray matter structures has functional connections with the cerebellum (superior colliculus, anterior pretectal nucleus, red nucleus, nucleus of posterior commissure, inferior olive, pontine, pontine reticular, and vestibular nuclei). The cerebellum itself shows parasagittal stripes of cadherin-8 expression in the Purkinje cell layer. In the hindbrain, cadherin-8 is expressed by several cranial nerve nuclei. Results from this study show that cadherin-8 expression in the embryonic and postnatal mouse brain is restricted to specific developing gray matter structures. These data support the idea that cadherins are a family of molecules whose expression provides a molecular code for the regionalization of the developing vertebrate brain.

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Microglial response to transient focal ischemia was examined using an immunohistochemical method with a monoclonal antibody to phosphotyrosine (P-Tyr). For this purpose, a rat model of reversible middle cerebral artery occlusion for 1 h was used. Compared with results in the noninsulted hemisphere, there was a significant increase in P-Tyr immunolabeling of the microglia in the insulted cerebral cortex 3 h postreperfusion. This microglial reaction progressed up to 24 h after ischemic insult. In the affected cerebral cortex, morphological changes of the microglial positive for P-Tyr were also observed, with shortened and thickened processes, enlarged cell bodies, and ameboid features. Cell density analysis did not show any apparent change in number of P-Tyr-positive microglia in the insulted cortex at 6, 12, and 24 h after reperfusion, suggesting that the cells with increased P-Tyr immunoreactivity were resident microglia. The present findings suggest that signal transduction mediated by tyrosine phosphorylation is involved in the microglial response to ischemic injury in the rat cerebral cortex.

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