Gamma-aminobutyric acid: role in primary afferent depolarization.
The effects of putative transmitters on the primary afferent terminals were studied in the magnesium-treated, isolated spinal cord of the frog. Gamma-aminobutyric acid and glutamic acid reversibly depolarized primary afferent terminals and increased their excitability, whereas glycine produced weak and variable effects. Bicuculline and picrotoxin, which reduce primary afferent depolarization, reversibly antagonized the gamma-aminobutyric acid-mediated responses but had little effect on those produced by either glutamic acid or glycine. The glutamic acid- and the gamma-aminobutyric acid-induced depolarizations remained in the absence of external chloride but disappeared in the absence of external sodium. These results support the hypotheses that gamma-aminobutyric acid is the transmitter mediating the synaptic depolarization of primary afferent terminals and that sodium is the predominant ion involved.
D000200:Action Potentials / Q000187:drug effects; D000470:Alkaloids / Q000494:pharmacology; D000613:Aminobutyrates / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000818:Animals; D001001:Anura; D004149:Dioxoles / Q000494:pharmacology; D004594:Electrophysiology / Q000187:drug effects*; D005971:Glutamates / Q000494:pharmacology; D005998:Glycine / Q000494:pharmacology; D066298:In Vitro Techniques; D007546:Isoquinolines / Q000494:pharmacology; D009475:Neurons, Afferent / Q000187:drug effects; D010852:Picrotoxin / Q000494:pharmacology; D011894:Rana pipiens; D013116:Spinal Cord / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects
D000470:Alkaloids; D000613:Aminobutyrates; D004149:Dioxoles; D005971:Glutamates; D005998:Glycine; D007546:Isoquinolines; D010852:Picrotoxin