Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA

• Published in: Nature neuroscience Vol. 15; no. 9; pp. 1195 - 1197
• Main Authors: Williams, Courtney, Chen, Wenyan, Lee, Chia-Hsueh, Yaeger, Daniel, Vyleta, Nicholas P, Smith, Stephen M
• Format: Journal Article
• Language: English
• Published: United States Nature Publishing Group 01.09.2012
• Subjects: Analysis of Variance; Animals; Calcium - metabolism; Calcium Channel Blockers; Calcium channels; Calcium Channels - physiology; Calcium Channels, N-Type - physiology; Calcium Channels, P-Type - physiology; Calcium Channels, Q-Type - physiology; Cells, Cultured; Cerebral Cortex - metabolism; Cerebral Cortex - physiology; Excitatory Postsynaptic Potentials - physiology; GABA; gamma-Aminobutyric Acid - metabolism; Mice; Patch-Clamp Techniques; Physiological aspects; Physiology; Synapses; Synaptic Transmission - physiology; Synaptic Vesicles - physiology; United States; Austria; Oregon; United States > US
• ISSN: 1097-6256; 1546-1726
• DOI: 10.1038/nn.3162

Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+) regulates spontaneous transmission is unclear. We found that VACCs are the major physiological triggers for spontaneous release at mouse neocortical inhibitory synapses. Moreover, despite the absence of a synchronizing action potential, we found that spontaneous fusion of a GABA-containing vesicle required the activation of multiple tightly coupled VACCs of variable type.