
doi: 10.1139/y80-032
pmid: 7378921
Injections of γ-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 α-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.
Motor Neurons, Aminoisobutyric Acids, Muscimol, Sodium, Glycine, Action Potentials, Membrane Potentials, Benzodiazepines, Cats, Animals, Neuroglia, gamma-Aminobutyric Acid
Motor Neurons, Aminoisobutyric Acids, Muscimol, Sodium, Glycine, Action Potentials, Membrane Potentials, Benzodiazepines, Cats, Animals, Neuroglia, gamma-Aminobutyric Acid
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