Abstract
We have already reported the occurrence of γ-aminobutyric acid (GABA) and glutamic acid decarboxylase and 3H-GABA uptake and release from the guinea pig urinary bladder. When we tested the effect of GABA on the motility and ACh release in the isolated urinary bladder O2 guinea pig, GABA inhibited dose-dependently, the cholinergic component of electrical stimulation (ES)- and nicotine-induced contractions, but not the non-cholinergic component of ES- and ACh-induced contractions. These effects of GABA were antagonized by bicuculline and furosemide. ES and nicotine evoked the tetrodotoxin-sensitive and Ca++-dependent release of 3H-ACh from the strips of urinary bladder preloaded with 3H-choline. Bicuculline at 10−5M enhanced the ACh release and contraction evoked by ES, under conditions of stimulation which produced a maximal release of GABA, -hereby suggesting that bicuculline antagonizes the inhibitory effect of endogenous GABA released during the stimulation. Nicotine-evoked release of ACh and contraction were inhibited by GABA and muscimol, but not by baclofen. These effects of 3ABA were antagonized by bicuculline and furosemide, but not by rhentolamine and propranolol. Thus, GABA may affect the motility of the guinea pig urinary bladder by inhibiting release of ACh through bicuculline-sensitive GABA receptors associated with the Cl- ion channel.
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