| First Author | Ramadan E | Year | 2003 |
| Journal | J Neurophysiol | Volume | 89 |
| Issue | 1 | Pages | 128-34 |
| PubMed ID | 12522165 | Mgi Jnum | J:102972 |
| Mgi Id | MGI:3608285 | Doi | 10.1152/jn.00700.2002 |
| Citation | Ramadan E, et al. (2003) GABA(A) receptor beta3 subunit deletion decreases alpha2/3 subunits and IPSC duration. J Neurophysiol 89(1):128-34 |
| abstractText | Deletion of the beta3 subunit of the GABA(A) receptor produces severe behavioral deficits and epilepsy. GABA(A) receptor-mediated miniature inhibitory postsynaptic currents (mIPSCs) in cortical neurons in cultures from beta3 -/- mice were significantly faster than those in beta3 +/+ mice and were more prolonged by zolpidem. Surface staining revealed that the number of beta2/3, alpha2, and alpha3 (but not of alpha1) subunit-expressing neurons and the intensity of subunit clusters were significantly reduced in beta3 -/- mice. Transfection of beta3 -/- neurons with beta3 cDNA restored beta2/3, alpha2, and alpha3 subunits immunostaining and slowed mIPSCs decay. We show that the deletion of the beta3 subunit causes the loss of a subset of GABA(A) receptors with alpha2 and alpha3 subunits while leaving a receptor population containing predominantly alpha1 subunit with fast spontaneous IPSC decay and increased zolpidem sensitivity. |
