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J Neurophysiol 89: 128-134, 2003; doi:10.1152/jn.00700.2002
0022-3077/03 $5.00
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J Neurophysiol (January 1, 2003). 10.1152/jn.00700.2002
Submitted on Submitted 19 August 2002; accepted in final form 24 September 2002

GABAA Receptor beta 3 Subunit Deletion Decreases alpha 2/3 Subunits and IPSC Duration

Epolia Ramadan,1 Zhanyan Fu,2 Gabriele Losi,2 Gregg E. Homanics,3 Joseph H. Neale,1 and Stefano Vicini2

 1Department of Biology,  2Department of Physiology and Biophysics, Georgetown University School of Medicine, Washington, DC 20057; and  3Departments of Anesthesiology and Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261

Ramadan, Epolia, Zhanyan Fu, Gabriele Losi, Gregg E. Homanics, Joseph H. Neale, and Stefano Vicini. GABAA Receptor beta 3 Subunit Deletion Decreases alpha 2/3 Subunits and IPSC Duration. J. Neurophysiol. 89: 128-134, 2003. Deletion of the beta 3 subunit of the GABAA receptor produces severe behavioral deficits and epilepsy. GABAA receptor-mediated miniature inhibitory postsynaptic currents (mIPSCs) in cortical neurons in cultures from beta 3 -/- mice were significantly faster than those in beta 3 +/+ mice and were more prolonged by zolpidem. Surface staining revealed that the number of beta 2/3, alpha 2, and alpha 3 (but not of alpha 1) subunit-expressing neurons and the intensity of subunit clusters were significantly reduced in beta 3 -/- mice. Transfection of beta 3 -/- neurons with beta 3 cDNA restored beta 2/3, alpha 2, and alpha 3 subunits immunostaining and slowed mIPSCs decay. We show that the deletion of the beta 3 subunit causes the loss of a subset of GABAA receptors with alpha 2 and alpha 3 subunits while leaving a receptor population containing predominantly alpha 1 subunit with fast spontaneous IPSC decay and increased zolpidem sensitivity.




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