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Cerebral Cortex Advance Access originally published online on April 10, 2009
Cerebral Cortex 2009 19(Supplement 1):i1-i10; doi:10.1093/cercor/bhp038
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© 2009 The Authors
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article appears in the following Cerebral Cortex issue: Cortical Development: Neural Stem Cells to Neural Circuits Chania, Greece, May 22-25, 2008 [View the issue table of contents]

Characterization of Nkx6-2-Derived Neocortical Interneuron Lineages

Vitor H. Sousa, Goichi Miyoshi, Jens Hjerling-Leffler, Theofanis Karayannis and Gord Fishell

Neuroscience Program, Smilow Research Center, New York University, New York, NY 10016, USA

Address correspondence to Dr Gordon Fishell, Smilow Neuroscience Program, 5th flr., Smilow Research Building, NYU School of Medicine, 522 1st Ave, New York, NY 10016, USA. Email: fisheg01{at}nyumc.org.

Ventral telencephalic progenitors expressing the homeodomain transcription factor Nkx6-2 have been shown to give rise to a multitude of cortical interneuron subtypes usually associated with origin in either the medial ganglionic eminence or the caudal ganglionic eminence. The function of Nkx6-2 in directing the fate of those progenitors has, however, not been thoroughly analyzed. We used a combination of genetic inducible fate mapping and in vivo loss-of-function to analyze the requirement of Nkx6-2 in determining the fate of cortical interneurons. We have found that interneuron subtypes are born with a characteristic temporal pattern. Furthermore, we extend the characterization of interneurons from the Nkx6-2 lineage through the application of electrophysiological methods. Analysis of these populations in Nkx6-2 null mice suggests that there is a small and partially penetrant loss of delayed non-fast spiking somatostatin/calretinin double positive cortical interneurons in the absence of Nkx6-2 gene function.

Key Words: genetic fate mapping • interganglionic sulcus • loss of function • mouse genetics • whole-cell physiology


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