RRC ID 37886
著者 Bannai H, Niwa F, Sherwood MW, Shrivastava AN, Arizono M, Miyamoto A, Sugiura K, Lévi S, Triller A, Mikoshiba K.
タイトル Bidirectional Control of Synaptic GABAAR Clustering by Glutamate and Calcium.
ジャーナル Cell Rep
Abstract GABAergic synaptic transmission regulates brain function by establishing the appropriate excitation-inhibition (E/I) balance in neural circuits. The structure and function of GABAergic synapses are sensitive to destabilization by impinging neurotransmitters. However, signaling mechanisms that promote the restorative homeostatic stabilization of GABAergic synapses remain unknown. Here, by quantum dot single-particle tracking, we characterize a signaling pathway that promotes the stability of GABAA receptor (GABAAR) postsynaptic organization. Slow metabotropic glutamate receptor signaling activates IP3 receptor-dependent calcium release and protein kinase C to promote GABAAR clustering and GABAergic transmission. This GABAAR stabilization pathway counteracts the rapid cluster dispersion caused by glutamate-driven NMDA receptor-dependent calcium influx and calcineurin dephosphorylation, including in conditions of pathological glutamate toxicity. These findings show that glutamate activates distinct receptors and spatiotemporal patterns of calcium signaling for opposing control of GABAergic synapses.
巻・号 13(12)
ページ 2768-80
公開日 2015-12-29
DOI 10.1016/j.celrep.2015.12.002
PII S2211-1247(15)01414-X
PMID 26711343
PMC PMC4700050
MeSH Animals Calcium / metabolism* Calcium Signaling GABAergic Neurons / metabolism GABAergic Neurons / physiology* Glutamic Acid / metabolism* Mice, Knockout Rats Rats, Wistar Receptors, GABA-A / metabolism* Synaptic Transmission / physiology*
IF 8.109
引用数 44
WOS 分野 CELL BIOLOGY
リソース情報
ヒト・動物細胞 HeLa(RCB0007)