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.
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Constanti et al. (1980) studied this question.
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