Increased asynchronous GABA release causes more inhibition in human epileptic brain?

• 来源期刊: 中国药理学报（英文版）
• 年，卷（期）: 2012,（7）
• 页码范围: 859-860
• 页数: 2页
• 语种: 英文
• DOI: 10.1038/aps.2012.92

摘要

When an action potential (AP) propagates to the presynaptic terminals,Ca2+ influx through voltage-gated Ca2+ channels triggers rapid synchronous transmitter release within milliseconds,which is then followed by a so-called asynchronous release with a prolonged time course of tens or hundreds of milliseconds at both excitatory and inhibitory synapses[1-3].Fast synchronous release is well-known as the foundation of precise neuronal communication,whereas the characteristics and functions of asynchronous release in central nervous system,especially in human brain,are largely unexplored.Jiang et al[4] now report that asynchronous release occurs in all GABAergic synapses of fast-spiking (FS) interneurons,and the strength of asynchronous GABA release increases in human epileptic neocortex,which may contribute to the regulation of epileptiform activities.