Stimulation of brain α7-nicotinic acetylcholine receptors suppresses the rat micturition through brain GABAergic receptors

Brain nicotinic acetylcholine receptors (nAChRs) reportedly suppress the micturition, but mechanisms responsible for this suppression remain unclear. We previously reported that intracerebroventricularly administered (±)-epibatidine (non-selective nAChR agonist) activated sympatho-adrenomedullary system, which can affect micturition. Therefore, we investigated (1) whether (±)-epibatidine-induced effects on micturition were dependent and (2) brain subtypes involved in urethane-anesthetized male Wistar rats. Plasma noradrenaline adrenaline (catecholamines) measured just before 5 min after administration. Evaluation of urodynamic parameters, intercontraction intervals (ICI) maximal voiding pressure (MVP) by cystometry was started 1 h administration or intracerebroventricular pretreatment with other drugs continued Intracerebroventricularly elevated plasma catecholamines prolonged ICI without affecting MVP, these changes suppressed pretreated mecamylamine antagonist). Acute bilateral adrenalectomy abolished elevation catecholamines, had no effect prolongation. The latter methyllycaconitine (selective α7-nAChR antagonist), SR95531 (GABAA SCH50911 (GABAB not dihydro-β-erythroidine α4β2-nAChR PHA568487 similar to (±)-epibatidine. These results suggest stimulation α7-nAChRs suppresses rat through GABAA/GABAB receptors, independently outflow modulation.