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The Journal of Neuroscience, February 1, 2006, 26(5):1646-1655; doi:10.1523/JNEUROSCI.3651-05.2006

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 Previous Article

Development/Plasticity/Repair
Layer Positioning of Late-Born Cortical Interneurons Is Dependent on Reelin But Not p35 Signaling

Vicki Hammond,¹ Eva So,¹ Jenny Gunnersen,¹ Helen Valcanis,¹ Michael Kalloniatis,² and Seong-Seng Tan¹

¹Howard Florey Institute, The University of Melbourne, Parkville 3010, Victoria, Australia, and ²Department of Optometry and Vision Science, University of Auckland, Auckland 1020, New Zealand

Correspondence should be addressed to Seong-Seng Tan, Brain Development Laboratory, Howard Florey Institute, The University of Melbourne, Parkville 3010, Victoria, Australia. Email: stan{at}hfi.unimelb.edu.au

We tested the response of interneurons to the absence of Reelin signaling or p35 in the mouse neocortex. We provide three independent strands of evidence to demonstrate that layering of late-born (but not early-born) interneurons is regulated by Reelin signaling. First, early-born and late-born interneurons behaved differently in mice lacking Reelin or disabled 1 (Dab1). Early-born interneurons showed layer inversion, whereas late-born interneurons did not demonstrate layer inversion but were randomly distributed across the cortex. Second, in p35 mutant brains (in which Reelin signaling is intact), late-born interneurons are appropriately positioned in the upper layers despite the malpositioning of all other cortical neurons in these mice. Third, transplanted late-born interneuron precursors (wild type) into Dab1^–/– cortices showed appropriate upper layer segregation. Together, these results indicate that, in the absence of Reelin signaling, late-born interneurons fail to laminate properly, and this is restored in an environment in which Reelin signaling is intact. These studies suggest different mechanisms for the stratification of cortical interneurons. Whereas the early-born interneurons appear to be associated with projection neuron layering, late-born interneurons rely on Reelin signaling for their correct lamination.

Key words: Reelin; disabled-1; p35; interneuron; migration; GABA

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Received Aug. 28, 2005; revised Nov. 10, 2005; accepted Dec. 21, 2005.

Correspondence should be addressed to Seong-Seng Tan, Brain Development Laboratory, Howard Florey Institute, The University of Melbourne, Parkville 3010, Victoria, Australia. Email: stan{at}hfi.unimelb.edu.au

This article has been cited by other articles:

				S. Rakic, Y. Yanagawa, K. Obata, C. Faux, J. G. Parnavelas, and M. Nikolic Cortical Interneurons Require p35/Cdk5 for their Migration and Laminar Organization Cereb Cortex, August 1, 2009; 19(8): 1857 - 1869. [Abstract] [Full Text] [PDF]

				G. Ying, S. Wu, R. Hou, W. Huang, M. R. Capecchi, and Q. Wu The Protocadherin Gene Celsr3 Is Required for Interneuron Migration in the Mouse Forebrain Mol. Cell. Biol., June 1, 2009; 29(11): 3045 - 3061. [Abstract] [Full Text] [PDF]

				K. Leto, A. Bartolini, Y. Yanagawa, K. Obata, L. Magrassi, K. Schilling, and F. Rossi Laminar Fate and Phenotype Specification of Cerebellar GABAergic Interneurons J. Neurosci., May 27, 2009; 29(21): 7079 - 7091. [Abstract] [Full Text] [PDF]

				R. Pla, V. Borrell, N. Flames, and O. Marin Layer acquisition by cortical GABAergic interneurons is independent of Reelin signaling. J. Neurosci., June 28, 2006; 26(26): 6924 - 6934. [Abstract] [Full Text] [PDF]

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