期刊
NATURE NEUROSCIENCE
卷 7, 期 5, 页码 525-533出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn1227
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资金
- Medical Research Council [G9603438] Funding Source: Medline
- Medical Research Council [G9603438] Funding Source: researchfish
- MRC [G9603438] Funding Source: UKRI
Synaptic inhibition is a vital component in the control of cell excitability within the brain. Here we report a newly identified form of inhibitory synaptic plasticity, termed depolarization-induced potentiation of inhibition, in rodents. This mechanism strongly potentiated synaptic transmission from interneurons to Purkinje cells after the termination of depolarization-induced suppression of inhibition. It was triggered by an elevation of Ca(2+) in Purkinje cells and the subsequent retrograde activation of presynaptic NMDA receptors. These glutamate receptors promoted the spontaneous release of Ca(2+) from presynaptic ryanodine-sensitive Ca(2+) stores. Thus, NMDA receptor-mediated facilitation of transmission at this synapse provides a regulatory mechanism that can dynamically alter the synaptic efficacy at inhibitory synapses.
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