Role of thalamic axons in the expression of H-2Z1, a mouse somatosensory cortex specific marker.

In the H-2Z1 mouse line, postnatal expression of the lacZ containing transgene in the cerebral cortex is restricted to layer IV neurons of the somatosensory area. We have used H-2Z1 embryos in previous heterotopic transplantation experiments to investigate the chronology of determination of areal identity. From the onset of neurogenesis, the cortex was regionalized in domains fated to express or not the somatosensory area-specific transgene. Determination occured 1 day later. In the present study, we show that, in vivo, H-2Z1 expression coincides with invasion of the cortical plate by thalamic afferents. We therefore investigated the role of thalamic innervation in the onset of H-2Z1 expression. For this purpose, we examined the pattern of H-2Z1 expression in perinatal cortical explant, in reeler mutant and MaoA deficient mice, or in animals which had received neonatal lesions affecting the somatosensory cortex or the thalamocortical projection. We found that, around birth, a switch occurs in the control of H-2Z1 expression: whereas H-2Z1 expression developed autonomously in embryonic parietal cortex in the absence of thalamic fibers, a transient requirement for a thalamic axon derived signal was observed postnatally. This property has interesting implications for the plasticity of cortical areas in development and evolution.