QBI Seminar: Mechanisms of diversification and allocation of cortical GABAergic interneurons
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- Professor Carlos Ibanez
Department of Physiology, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore
Abstract:
Axon guidance and neuronal migration share common molecular and cellular mechanisms. They are exquisitely coordinated in space and time to ensure appropriate formation of neural circuits. The thalamocortical projection, one of the most prominent tracts in the forebrain, and neocortical interneurons, the farthest-reaching migratory cell population in the developing telencephalon, share a similar trajectory, site of entry in the neocortex and timing of cortical invasion during development, suggesting that GABAergic interneuron migration and thalamocortical axon pathfinding may be interdependent and/or share common signals. Interneurons of the mammalian neocortex are generated in transient neurogenic structures of the embryonic ventral forebrain. As the developing brain expands, interneurons migrate tangentially to the overlying neocortex over a period of several days in the mouse. After their tangential dispersion throughout cortical areas, interneurons switch their mode of migration from tangential to radial and invade the cortical plate. Despite significant progress in the identification of signals that control tangential migration of cortical interneurons, the mechanisms that regulate their radial dispersion and laminar distribution are basically unknown. In this study, we tested the hypothesis that thalamocortical axons may provide guidance to MGE-derived GABAergic interneurons for their tangential migration to the neocortex and subsequent radial dispersion and cortical invasion. First, we compared the laminar distribution of interneurons in primary and secondary cortices, which differ in the type and pattern of thalamic innervation they receive. Subsequently, we studied interneuron distribution and migration in the neocortex of a mutant mouse that lacks thalamocortical axons as a consequence of abnormal thalamic development. This study provides some of the first insights into the mechanisms controlling radial dispersion of interneurons in the neocortex, and presents a new rationale for the coordinated invasion of the neocortex by GABAergic interneurons and thalamocortical axons.
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