RIM-BP2 regulates Ca2+ channel abundance and neurotransmitter release at hippocampal mossy fiber terminals

Author:

Miyano Rinako1ORCID,Sakamoto Hirokazu2ORCID,Hirose Kenzo23ORCID,Sakaba Takeshi1ORCID

Affiliation:

1. Graduate School of Brain Science, Doshisha University, Kyotanabe-shi, Kyoto 610-0394, Japan

2. Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan

3. International Research Center for Neurointelligence (WPI-IRCN), The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan

Abstract

Synaptic vesicles dock and fuse at the presynaptic active zone (AZ), the specialized site for transmitter release. AZ proteins play multiple roles such as recruitment of Ca 2+ channels as well as synaptic vesicle docking, priming and fusion. However, the precise role of each AZ protein type remains unknown. In order to dissect the role of RIM-BP2 at mammalian cortical synapses having low release probability, we applied direct electrophysiological recording and super-resolution imaging to hippocampal mossy fiber terminals of RIM-BP2 KO mice. By using direct presynaptic recording, we found the reduced Ca 2+ currents. The measurements of EPSCs and presynaptic capacitance suggested that the initial release probability was lowered because of the reduced Ca 2+ influx and impaired fusion competence in RIM-BP2 KO. Nevertheless, larger Ca 2+ influx restored release partially. Consistent with presynaptic recording, STED microscopy suggested less abundance of P/Q-type Ca 2+ channels at AZs deficient in RIM-BP2. Our results suggest that the RIM-BP2 regulates both Ca 2+ channel abundance and transmitter release at mossy fiber synapses.

Publisher

eLife Sciences Publications, Ltd

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