期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 40, 页码 15581-15586出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0800621105
关键词
GABAergic interneurons; basket cells; hippocampus; Ca2+ sensor
资金
- Deutsche Forschungsgemeinschaft [SFB 505, SFB 780, GRK 843]
- Leibniz Program
Previous studies revealed that synaptotagmin 1 is the major Ca2+ sensor for fast synchronous transmitter release at excitatory synapses. However, the molecular identity of the Ca2+ sensor at hippocampal inhibitory synapses has not been determined. To address the functional role of synaptotagmin 1 at identified inhibitory terminals, we made paired recordings from synaptically connected basket cells (BCs) and granule cells (GCs) in the dentate gyrus in organotypic slice cultures from wild-type and synaptotagmin 1-deficient mice. As expected, genetic elimination of synaptotagmin 1 abolished synchronous transmitter release at excitatory GC-BC synapses. However, synchronous release at inhibitory BC-GC synapses was maintained. Quantitative analysis revealed that elimination of synaptotagmin 1 reduced release probability and depression but maintained the synchrony of transmitter release at BC-GC synapses. Elimination of synaptotagmin 1 also increased the frequency of both miniature excitatory postsynaptic currents (measured in BCs) and miniature inhibitory postsynaptic currents (recorded in GCs), consistent with a clamping function of synaptotagmin 1 at both excitatory and inhibitory terminals. Single-cell reverse-transcription quantitative PCR analysis revealed that single BCs coexpressed multiple synaptotagmin isoforms, including synaptotagmin 1-5, 7, and 11-13. Our results indicate that, in contrast to excitatory synapses, synaptotagmin 1 Is not absolutely required for synchronous release at inhibitory BC-GC synapses. Thus, alternative fast Ca2+ sensors contribute to synchronous release of the inhibitory transmitter GABA in cortical circuits.
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