Modulation of gamma-[3H]aminobutyric acid release from rat cortical slices by alpha 2-adrenoceptors.
Modulation of gamma-aminobutyric acid (GABA) release by alpha 2-adrenoceptor agonists has not been consistently demonstrated. This could be due to high levels of norepinephrine (NE) concomitantly evoked by stimulation parameters needed for GABA release. In the present experiments, NE release was preferentially decreased by omission of calcium (Ca2+) and alpha 2-modulation of [3H]GABA release from cortical slices was measured. The antagonist rauwolscine increased only Ca2+-dependent [3H]GABA release, while the agonists guanabenz and clonidine inhibited only Ca2+-independent GABA release. These results suggest that release of endogenous NE diminished the effect of alpha 2-agonists but reveals the effect of antagonists and support the hypothesis that endogenous NE inhibits GABA release in cortex.
Peris
J
J
Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262.
Harris
R A
RA
Zahniser
N R
NR
D000818:Animals; D002118:Calcium / Q000502:physiology; D003000:Clonidine / Q000494:pharmacology; D006143:Guanabenz / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D009778:Occipital Lobe / Q000378:metabolism*; D010296:Parietal Lobe / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D005680:gamma-Aminobutyric Acid; D006143:Guanabenz; D003000:Clonidine; D002118:Calcium; D009638:Norepinephrine