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Intrinsically determined cell death of developing cortical interneurons

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Intrinsically determined cell death of developing cortical interneurons

dc.contributor.author	Southwell, Derek G.	es_ES
dc.contributor.author	Paredes, Mercedes F.	es_ES
dc.contributor.author	Galvao, Rui P.	es_ES
dc.contributor.author	Jones, Daniel L.	es_ES
dc.contributor.author	Froemke, Robert C.	es_ES
dc.contributor.author	Sebe, Joy Y.	es_ES
dc.contributor.author	Alfaro Cervelló, Clara	es_ES
dc.contributor.author	Tang, Yunshuo	es_ES
dc.contributor.author	García Verdugo, José Manuel	es_ES
dc.contributor.author	Rubenstein, John L.	es_ES
dc.contributor.author	Baraban, Scott C.	es_ES
dc.contributor.author	Alvarez-Buylla, Arturo	es_ES
dc.date.accessioned	2015-06-19T10:19:54Z
dc.date.available	2015-06-19T10:19:54Z
dc.date.issued	2012	es_ES
dc.identifier.citation	Nature Vol. 491 Issue 7422: pp. 109-113	es_ES
dc.identifier.uri	http://hdl.handle.net/10550/44561
dc.description.abstract	Cortical inhibitory circuits are formed by GABAergic interneurons, a cell population that originates far from the cerebral cortex in the embryonic ventral forebrain. Given their distant developmental origins, it is intriguing how the number of cortical interneurons is ultimately determined. One possibility, suggested by the neurotrophic hypothesis1-5, is that cortical interneurons are overproduced, and then following their migration into cortex, excess interneurons are eliminated through a competition for extrinsically derived trophic signals. Here we have characterized the developmental cell death of mouse cortical interneurons in vivo, in vitro, and following transplantation. We found that 40% of developing cortical interneurons were eliminated through Bax- (Bcl-2 associated X-) dependent apoptosis during postnatal life. When cultured in vitro or transplanted into the cortex, interneuron precursors died at a cellular age similar to that at which endogenous interneurons died during normal development. Remarkably, over transplant sizes that varied 200-fold, a constant fraction of the transplanted population underwent cell death. The death of transplanted neurons was not affected by the cell-autonomous disruption of TrkB (tropomyosin kinase receptor B), the main neurotrophin receptor expressed by central nervous system (CNS) neurons6-8. Transplantation expanded the cortical interneuron population by up to 35%, but the frequency of inhibitory synaptic events did not scale with the number of transplanted interneurons. Together, our findings indicate that interneuron cell death is intrinsically determined, either cell-autonomously, or through a population-autonomous competition for survival signals derived from other interneurons.	es_ES
dc.title	Intrinsically determined cell death of developing cortical interneurons	es_ES
dc.type	journal article	es_ES
dc.identifier.doi	10.1038/nature11523	es_ES
dc.identifier.idgrec	085202	es_ES