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RIM-BP2 regulates Ca 2+ channel abundance and neurotransmitter release at hippocampal mossy fiber terminals.

Rinako MiyanoHirokazu SakamotoKenzo HiroseTakeshi Sakaba
Published in: eLife (2024)
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 knockout (KO) mice. By using direct presynaptic recording, we found the reduced Ca 2+ currents. The measurements of excitatory postsynaptic currents (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.
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