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

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 ^1,2,3 . 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.