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The Release of γ‐Aminobutyric Acid, Glutamate, and Acetylcholine from Striatal Slices: A Mass Fragmentographic Study
Author(s) -
Moroni F.,
Bianchi C.,
Tanganelli S.,
Moneti G.,
Beani L.
Publication year - 1981
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1981.tb00420.x
Subject(s) - acetylcholine , tetrodotoxin , glutamate receptor , neurotransmitter , chemistry , stimulation , medicine , endocrinology , efflux , glutamine , liberation , microdialysis , striatum , dopamine , biology , biochemistry , amino acid , central nervous system , in vitro , receptor
Abstract: The release processes of endogenous Acetylcholine (ACh), γ‐aminobutyric acid (GABA), glutamate (Glu) and glutamine (GLN) were studied in superfused guinea‐pig caudatal slices. Basal ACh release remained constant for up to 2 h, while the basal release of GABA, Glu and GLN declined to half or less of its initial values after 1 h of superfusion. Electrical stimulation increased the ACh release by 700–800% and that of GABA by 80% whereas it decreased the output of Glu by 50% and failed to modify the GLN efflux. KCl (25 mM) increased the output of ACh by 400%, that of GABA by approximately 500% and decreased that of Glu by 40%. Substituting of CaCl 2 by MgCl 2 in the superfusion medium reduced the basal ACh release by 70% whereas no differences were observed in the basal efflux of GABA, Glu and GLN. Under these conditions, no evoked release of ACh or of GABA was detected, following electrical or KCl stimulation. Tetrodotoxin 5 × 10 ‐7 M decreased the basal ACh release by 60% and increased the GABA efflux by 40%. The toxin abolished the stimulus‐evoked ACh efflux but scarcely affected that of GABA. These results are consistent with a possible neurotransmitter role of ACh and GABA in the striatum and show some differences in the ionic mechanisms underlying GABA and ACh release.