Central neurotransmitter mechanisms involved in the control of urinary bladder function. An experimental study in the rat.

Central neurotransmitter systems have been activated in anaesthetized rats, while the effects on the urinary bladder have been recorded by cystometric procedures. Stimulation of central catecholamine neurons with the amine precursor L-3,4-dihydroxyphenylalanine (L-DOPA), after peripheral inhibition of the degradating enzyme dopadecarboxylase, resulted in a hyperactive urinary bladder response. This bladder action seems to be elicited mainly via central dopamine receptors, and mediated via neurons of non-catecholamine type. Activation of central muscarinic receptors with oxotremorine, after pretreatment with methylscopolamine, induced a hyperactive urinary bladder response, which is suggested to originate in pontine-mesencephalic structures as well. There might in some instances be an interaction with muscarinic receptors in the generation of the bladder hyperreactivity to L-DOPA, at the pontine-mesencephalic brain level. The bladder response to stimulation of central muscarinic receptors, on the other hand, seems to be independent of intact adrenergic neurons. The peripheral mediation of the bladder response to L-DOPA is propagated via the pelvic nerves; in the peripheral ganglia via cholinergic receptors, but in the bladder detrusor via non-cholinergic as well as non-adrenergic receptors. Activation of central GABA mechanisms with GABA, muscimol and diazepam strongly inhibited the bladder hyperactivity to L-DOPA. This inhibition probably occurred in the pontine-mesencephalic brain area. The results suggest that excitatory dopaminergic and muscarinic receptors, as well as inhibitory gabaergic receptors in the pontine-mesencephalic brain region, are involved in the modulation of the urinary bladder function.