Inhibition facilitates depression

摘要

The release of the inhibitory neuro-transmitter y-aminobutyric acid (GABA) and the subsequent activation of Iigand-gated GABAA receptors (GABAAR) and G protein-coupled GABAB receptors (GABABR) is generally thought to, as the name implies, inhibit neurons. On the postsynaptic side, the inhibition produced by GABABR activation is in part mediated by the opening of G protein-coupled inward rectifying potassium (GIRK) channels (Gahwiler & Brown, 1985). Functionally, synaptic activation of GABABR produces a long-lasting (~400 ms) window of inhibition in a large population of postsynaptic neurons when presynaptic neurons are coherently activated (Scanziani, 2000)