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Ion Channels and Excitable Membranes

開催日 2014/9/12
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Cav2 channel subtype-dependent Ca2+ nano-/micro-domain signaling at rat cerebellar granule cell axons

  • P2-005
  • 佐竹 伸一郎 / Shin 'ichiro Satake:1,2 井本 敬二 / Keiji Imoto:1,2 
  • 1:自然科学研究機構・生理研・生体情報 / National Institute for Physiological Sciences (NIPS), Okazaki, Japan 2:総研大・生命科学 / The Graduate University for Advanced Studies (SOKENDAI), Okazaki, Japan 

We previously reported that paired-pulse activation of rat cerebellar granule cell (GC) ascending axon fibers at short intervals (30-100 ms) causes not only facilitation of the peak amplitude (PPFamp) of the second EPSC (EPSC2) recorded from molecular layer interneurons (MLIs) but also prolongation of the EPSC2 decay time (PPPdecay) relative to those of the first EPSC (EPSC1). PPFamp is the result of transient increases in release probability and multivesicular release (MVR). In contrast, PPPdecay is elicited by an increase in MVR and the subsequent pooling of MVR glutamate among adjacent active synapses as well as by a delayed release. We here report that (i) Cav2.1 and Cav2.2 channels differentially regulate PPPdecay and PPFamp and (ii) the topographical distance between Cav2.1 channels and exocytotic Ca2+ sensors plays an important role in eliciting MVR. The amplitude of GC-MLI EPSCs decreased after application of the membrane-permeable slow Ca2+ chelator EGTA-AM. This decrease was stronger for EPSC2, thereby reducing PPFamp significantly. In addition, EGTA-AM reduced τdecay of EPSC2, resulting in the suppression of PPPdecay. It is therefore probable that Ca2+ sensors that mediate MVR are located more distally from Cav2.1 channels and Ca2+ accumulates even at release sites distant from the open channel. We further compared the effect of subtype-selective Cav2 channel blockers on GC-MLI EPSCs after treatment with EGTA-AM. ω-Agatoxin IVA and ω-conotoxin GVIA similarly reduced the amplitude of EPSC1 with a clear enhancement of PPFamp. These Cav2 blockers did not cause any significant changes in PPPdecay after EGTA-AM treatment. Thus, Cav2.1 and Cav2.2 channels appeared to have similar impacts on transmitter release at the GC ascending axons when the accumulation of free Ca2+ and the following activation of distally located Ca2+ sensors (i.e., microdomain signaling) were suppressed.

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