Extracellular Ca2+ Directly Inhibits Exocytosis in Neurons - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Biophysical Journal Année : 2011

Extracellular Ca2+ Directly Inhibits Exocytosis in Neurons

Wei Xiong
  • Fonction : Auteur
  • PersonId : 1020667
Tao Liu
Yeshi Wang
  • Fonction : Auteur
Xaiowei Chen
  • Fonction : Auteur
Lei Sun
  • Fonction : Auteur
Ning Guo
  • Fonction : Auteur
Hui Zheng
  • Fonction : Auteur
Lianghong Zheng
  • Fonction : Auteur
Weiping Han
  • Fonction : Auteur
Claire xi Zhang
  • Fonction : Auteur
Zhuan Zhou
  • Fonction : Auteur

Résumé

Exocytosis of transmitter releasing vesicles is elicited by an elevation of intracellular Ca2+ concentration ([Ca2+]i). Given the existing Ca2+ sensor receptor (CaSR), although [Ca2+]i-induced exocytosis is fully established, however, whether extracellular Ca2+ (concentration [Ca2+]o) directly regulates exocytosis is not rigorously examined yet. Here we report that extracellular Ca2+ inhibited exocytosis following moderate [Ca2+]i rises (2-3 μM), which were triggered by either photolysis of caged Ca2+ or caffeine. IC50 of extracellular Ca2+ inhibition on exocytosis (ECIE) was 1.38 mM, so that a physiological reduction (∼30%) of [Ca2+]o significantly increased the evoked exocytosis. On single vesicle level, the quantal size and release frequency were significantly regulated by physiological [Ca2+]o. Involvement of CaSR in ECIE was excluded by experiments of pharmacology and molecular biology. Thus, as an extension of the classic Ca2+ hypothesis of synaptic release, physiological extracellular Ca2+ plays dual roles in evoked exocytosis by providing source of Ca2+ influx, and by directly regulating quantal size and release probability in neuronal cells.

Dates et versions

hal-01710262 , version 1 (15-02-2018)

Identifiants

Citer

Wei Xiong, Tao Liu, Yeshi Wang, Xaiowei Chen, Lei Sun, et al.. Extracellular Ca2+ Directly Inhibits Exocytosis in Neurons. Biophysical Journal, 2011, 100 (3), pp.185a - 186a. ⟨10.1016/j.bpj.2010.12.1232⟩. ⟨hal-01710262⟩

Collections

CNRS
16 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More