Neuronal GABA release and GABA inhibition of ACh release in guinea pig urinary bladder

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Abstract
GABA and glutamate decarboxylase (GAD) are present in the urinary bladder of guinea pigs and the possible correlation in regional distribution between GABA, GAD and the number of vesical ganglion cells was studied. Electrical stimulation of the bladder strips produced an increase in the Ca-dependent and tetrodotoxin-sensitive [3H]GABA release and contractions in the strips preloaded with [3H]GABA. Nicotine, acetylcholine chloride (ACh) and hexamethonium did not significantly alter the release of [3H]GABA. Bicuculline significantly enhanced [3H]ACh release and cholinergic components of contractions evoked by electrical stimulation of the bladder strips preloaded with [3H]choline, suggesting that this compound antagonizes the effect of endogenous GABA released during stimulation. GABA and muscimol but not baclofen reduced both the [3H]ACh release and contractions evoked by nicotine. These effects of GABA were antagonized by bicuculline and furosemide, but not by .alpha.- and .beta.-adrenergic blockers. GABA may be a noncholinergic nonadrenergic inhibitory neurotransmitter in the urinary bladder. The motility of the urinary bladder is thus inhibited by reducing the release of ACh from the postganglionic cholinergic neurons through bicuculline-sensitive GABA receptors probably associated with the Cl ion channel.