Some functional consequences of GABA uptake by brain cells.
Recent electrophysiological studies on the rat hippocampus (in vivo and in vitro) provide further evidence that neuronal and glial uptake of the inhibitory transmitter gamma-aminobutyric acid (GABA) limits the intensity and the duration of effects not only of locally applied exogenous GABA but also of GABAergic inhibitory synaptic potentials (IPSPs). There is good reason to believe that such uptake is at least partly responsible for the 'fading' of GABA action. Moreover, because it is probably driven by the transmembrane Na+ electrochemical gradient and is accompanied by Na+ influx, GABA uptake is potentially electrogenic and therefore may have a depolarizing effect on both neurons and glia.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D009433:Neural Inhibition / Q000187:drug effects; D009457:Neuroglia / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013569:Synapses / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000378:metabolism* / Q000494:pharmacology
D005680:gamma-Aminobutyric Acid; D012964:Sodium