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Uptake and stimulus‐evoked release of [ 3 H]‐γ‐aminobutyric acid by myenteric nerves of guinea‐pig intestine
Author(s) -
Kerr D.I.B.,
Krantis A.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb09391.x
Subject(s) - myenteric plexus , tetrodotoxin , nipecotic acid , stimulation , veratridine , gabaergic , gamma aminobutyric acid , enteric nervous system , guinea pig , medicine , aminooxyacetic acid , chemistry , endocrinology , biology , biophysics , neurotransmitter , biochemistry , inhibitory postsynaptic potential , central nervous system , sodium , receptor , immunohistochemistry , organic chemistry , sodium channel , enzyme
1 Following preloading with [ 3 H]‐γ‐aminobutyric acid ([ 3 H]‐GABA), in the presence of β‐alanine to inhibit glial uptake of the label, electrical stimulation caused a frequency‐dependent release of tritium as [ 3 H]‐GABA from isolated longitudinal‐muscle myenteric‐plexus preparations of the guinea‐pig ileum and colon. 2 The electrically evoked efflux of [ 3 H]‐GABA was Ca 2+ ‐dependent, virtually abolished by preventing neuronal conduction with tetrodotoxin, and markedly reduced by preloading with [ 3 H]‐GABA in the presence of nipecotic acid which is an inhibitor of high affinity GABA‐uptake. Veratridine and KCl were less effective than electrical stimulation in evoking [ 3 H]‐GABA release. 3 It is concluded that the electrically stimulated efflux of [ 3 H]‐GABA originated from GABAergic neurones of the myenteric plexus which had taken up the label. 4 These results provide further evidence to support the suggestion that GABA is a transmitter in the mammalian enteric nervous system.