Nicotinic acetylcholine receptors in the autonomic control of bladder function

• Published in: European journal of pharmacology 2000-03, Vol.393 (1), p.137-140
• Main Authors: De Biasi, Mariella, Nigro, Filippo, Xu, Wei
• Format: Article
• Language: English
• Subjects: Animals; Autonomic dysfunction; Autonomic Nervous System - physiology; Biological and medical sciences; Bladder; Fundamental and applied biological sciences. Psychology; Knockout mice; Mice; Mice, Knockout; Nicotinic receptor; Nicotinic receptor subunit; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Receptors, Nicotinic - deficiency; Receptors, Nicotinic - physiology; Urinary Bladder - physiology; Vertebrates: nervous system and sense organs; Vertebrates: urinary system
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(00)00008-X

Micturition is achieved through complex neurological mechanisms involving somatic, autonomic and central components. This article briefly reviews recent findings on the autonomic control of urinary bladder function. Neuronal nicotinic acetylcholine receptors mediate fast synaptic transmission in autonomic ganglia, and activation of nicotinic receptors in parasympathetic bladder neurons produces contraction of the destrusor muscle. Autonomic ganglia contain transcripts for the α 3, α 4, α 5, α 7, β 2 and β 4 nicotinic subunits, which can assemble to form multiple nicotinic receptor subtypes, but the exact nicotinic receptor subunit composition in bladder ganglia is unknown. Mutant mice lacking the α 3 or the β 2 and the β 4 nicotinic subunits have enlarged bladders with dribbling urination and develop urinary infection and bladder stones. Bladder strips from α 3 null mice do not respond to nicotine but contract when stimulated with a muscarinic agonist or electric field stimulation. Mice lacking the β 2 subunit have no overt bladder phenotype, and their bladders contract in response to nicotine. Surprisingly, bladder strips from β 4 mutant mice do not respond to nicotine despite the absence of major bladder dysfunction in vivo. These findings suggest that nicotinic receptors containing the α 3 and the β 4 subunits are necessary for normal bladder function.