Channel-mediated release of glutamate from astrocytes via Bestrophin-1 potentiates synaptic strength
- Channel-mediated release of glutamate from astrocytes via Bestrophin-1 potentiates synaptic strength
- 한경석; 박형주; 서진수; 오수진; 윤보은; 조숙희; 우준성; 김혜연; 우동호; Rolando Berlinguer; Guido Mannaioni; Stephen F. Traynelis; 최세영; 이창준
- Issue Date
- Society For Neuroscience
- Recent studies have revealed that astrocytes regulate neuronal activity by releasing excitatory amino acid such as glutamate in Ca2+ dependent manner. Although Ca2+-dependent vesicular glutamate release mechanism in astrocyte has been suggested, the mechanism of astrocytic glutamate release through a channel has not been directly tested yet. Here we report that hippocampal CA1 astrocytes display a novel glutamate release mechanism via large-anion-permeable Ca2+ activated anion channels (CAAC). We found that putative CAAC, Bestrophin-1 (Best1) is able to permeate glutamate in Ca2+ dependent manner. Using the agonist (TFLLR peptide) for glia-specific Gq-coupled receptor (PAR-1) in hippocampal CA1, we found that PAR-1 activation induces glutamate release through Best1 in Ca2+ dependent manner. To verify the function of astrocytic glutamate, we performed a detailed electrophysiological analysis from hippocampal slices using cell type specific lentiviral shRNA expression system to selectively knockdown astrocytic or neuronal Best1. We demonstrated that astrocytic Best1-mediated glutamate activates neuronal NMDARs and induces the potentiation of hippocampal synaptic activity by NMDAR-dependent manner.
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