Intraneuronal effects of inhibitory amino acids.
Injections of gamma-aminobutyric acid (GABA) into spinal motoneurons (in cats under Dial) induce a small but relatively prolonged hyperpolarization (mean - 1.7 mV, SD 2.1; n = 25) which is associated with a rise in input resistance (mean 44%, SD 122; n = 34), is not reversed by hyperpolarization, and is not potentiated by intracellular release of benzodiazepines. Muscimol sometimes has a comparable effect, but alpha-aminoisobutyric acid and glycine do not. These observations are consistent with the possibility that motoneurons have a Na+-coupled GABA transport mechanism that is electrogenic and can be reversed by an excess of intracellular GABA.
D000200:Action Potentials / Q000187:drug effects; D000621:Aminoisobutyric Acids / Q000494:pharmacology; D000818:Animals; D001569:Benzodiazepines / Q000494:pharmacology; D002415:Cats; D005998:Glycine / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects* / Q000502:physiology; D009118:Muscimol / Q000494:pharmacology; D009457:Neuroglia / Q000187:drug effects; D012964:Sodium / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism / Q000494:pharmacology*
D000621:Aminoisobutyric Acids; D001569:Benzodiazepines; D009118:Muscimol; D005680:gamma-Aminobutyric Acid; D012964:Sodium; D005998:Glycine