期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 24, 期 2, 页码 442-450出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S1044-7431(03)00202-1
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资金
- NIMH NIH HHS [R01 MH060989-04, R01 MH060989-03, R01 MH062391-01A2, MH60989, R01 MH062391-03, MH62391, R01 MH062391-02, R01 MH060989-02, R01 MH060989-01A2] Funding Source: Medline
The gamma2 subunit of GABA(A) receptor chloride channels is required for normal channel function and for postsynaptic clustering of these receptors during synaptogenesis. In addition, GABA(A) receptor function is thought to contribute to normal postnatal maturation of neurons. Loss of postsynaptic GABA(A) receptors in gamma2-deficient neurons might therefore reflect a deficit in maturation of neurons due to the reduced channel function. Here, we have used the Cre-loxP strategy to examine the clustering function of the gamma2 subunit at mature synapses. Deletion of the gamma2 subunit in the third postnatal week resulted in loss of benzodiazepine-binding sites and parallel loss of punctate immunoreactivity for postsynaptic GABA(A) receptors and gephyrin. Thus, the gamma2 subunit contributes to postsynaptic localization of GABA(A) receptors and gephyrin by a mechanism that is operant in mature neurons and not limited to immature neurons, roost likely through interaction with proteins involved in trafficking of synaptic GABA(A) receptors. (C) 2003 Elsevier Inc. All rights reserved.
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