Journal
JOURNAL OF NEUROPHYSIOLOGY
Volume 89, Issue 1, Pages 128-134Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00700.2002
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Funding
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P01GM047818, R01GM052035] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [K02MH001680, R01MH064797] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038080] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R37AA010422, R01AA010422] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA002997] Funding Source: NIH RePORTER
- NIAAA NIH HHS [AA-10422] Funding Source: Medline
- NIDA NIH HHS [DA-02997] Funding Source: Medline
- NIGMS NIH HHS [GM-52035, GM-47818] Funding Source: Medline
- NIMH NIH HHS [MH-64797, MH-01680] Funding Source: Medline
- NINDS NIH HHS [NS-38080] Funding Source: Medline
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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.
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