Abstract
The establishment of connectivity between specific thalamic nuclei and cortical areas involves a dynamic interplay between the guidance of thalamocortical axons and the elaboration of cortical areas in response to appropriate innervation. We show here that Sema6A mutants provide a unique model to test current ideas on the interactions between subcortical and cortical guidance mechanisms and cortical regionalization. In these mutants, axons from the dorsal lateral geniculate nucleus (dLGN) are misrouted in the ventral telencephalon. This leads to invasion of presumptive visual cortex by somatosensory thalamic axons at embryonic stages. Remarkably, the misrouted dLGN axons are able to find their way to the visual cortex via alternate routes at postnatal stages and reestablish a normal pattern of thalamocortical connectivity. These findings emphasize the importance and specificity of cortical cues in establishing thalamocortical connectivity and the spectacular capacity of the early postnatal cortex for remapping initial sensory representations.
Highlights
A dynamic interplay exists between the processes of cortical arealization and those controlling the guidance and targeting of thalamocortical projections [1,2,3,4,5]
Broad injections of DiI in the thalamus at E15.5 revealed a prominent derailment of thalamic axons at the surface of the ventral telencephalon and amygdala in Sema6AÀ/À embryos (n 1⁄4 4/4; Figure 2D and 2G–2I), compared to the normal route of navigation through the internal capsule towards the neocortex observed in wild-type embryos
Many dorsal lateral geniculate nucleus (dLGN) axons are able to find their way to visual cortex during early postnatal stages, following alternate routes, and can establish almost normal patterns of thalamocortical connectivity in the adult
Summary
A dynamic interplay exists between the processes of cortical arealization and those controlling the guidance and targeting of thalamocortical projections [1,2,3,4,5] In development, both the thalamic field and the cortical sheet appear homogeneous in cytoarchitecture, and connections between them form in a smoothly topographic fashion, with dorsolateral thalamus projecting to caudal cortex and ventromedial thalamus to rostral cortex [6,7,8]. In mutants in the transcription factor Ebf or in the Dlx1/Dlx double mutants, a subset of thalamic axons is misrouted ventrally, resulting in a caudal shift of the remaining axons within the ventral telencephalon [16] This shift is projected onto the cortex so that at birth, caudal cortical areas are contacted by axons that would normally project to more rostral areas. The ultimate effect of this derangement on thalamocortical connectivity could not be assessed in these mutants, as they die perinatally
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