Bidirectional Control of Synaptic GABAAR Clustering by Glutamate and Calcium

Hiroko Bannai, Fumihiro Niwa, Mark W. Sherwood, Amulya Nidhi Shrivastava, Misa Arizono, Akitoshi Miyamoto, Kotomi Sugiura, Sabine Lévi, Antoine Triller*, Katsuhiko Mikoshiba

*この研究の対応する著者

研究成果: Article査読

58 被引用数 (Scopus)

抄録

GABAergic synaptic transmission regulates brain function by establishing the appropriate excitationinhibition (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.

本文言語English
ページ(範囲)2768-2780
ページ数13
ジャーナルCell Reports
13
12
DOI
出版ステータスPublished - 2015
外部発表はい

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学(全般)

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