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First published online October 26, 2007
doi: 10.1242/10.1242/dev.008524

Development 134, 4083-4093 (2007)
Published by The Company of Biologists 2007
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Selective cortical interneuron and GABA deficits in cyclin D2-null mice

Sara B. Glickstein1, Holly Moore2,3, Bozena Slowinska1, Joelle Racchumi1, Minah Suh4, Nao Chuhma2,3 and M. Elizabeth Ross1,*

1 Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA.
2 Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
3 The New York State Psychiatric Institute, New York, NY 10032, USA.
4 Department of Neurosurgery, Weill Cornell Medical College, New York, NY 10065, USA.

* Author for correspondence (e-mail: mer2005{at}med.cornell.edu)

Accepted 31 August 2007

In contrast to cyclin D1 nulls (cD1-/-), mice without cyclin D2 (cD2-/-) lack cerebellar stellate interneurons; the reason for this is unknown. In the present study in cortex, we found a disproportionate loss of parvalbumin (PV) interneurons in cD2-/- mice. This selective reduction in PV subtypes was associated with reduced frequency of GABA-mediated inhibitory postsynaptic currents in pyramidal neurons, as measured by voltage-clamp recordings, and increased cortical sharp activity in the EEGs of awake-behaving cD2-/- mice. Cell cycle regulation was examined in the medial ganglionic eminence (MGE), the major source of PV interneurons in mouse brain, and differences between cD2-/- and cD1-/- suggested that cD2 promotes subventricular zone (SVZ) divisions, exerting a stronger inhibitory influence on the p27 Cdk-inhibitor (Cdkn1b) to delay cell cycle exit of progenitors. We propose that cD2 promotes transit-amplifying divisions in the SVZ and that these ensure proper output of at least a subset of PV interneurons.

Key words: Cyclin D2 (Ccnd2), Parvalbumin interneurons, Cell cycle, Cortical excitability






© The Company of Biologists Ltd 2007