TY - JOUR T1 - Both nicotinic and muscarinic agonists acutely increase tyrosine 3-monooxygenase activity in the superior cervical ganglion. JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 280 LP - 283 VL - 223 IS - 2 AU - N Y Ip AU - R L Perlman AU - R E Zigmond Y1 - 1982/11/01 UR - http://jpet.aspetjournals.org/content/223/2/280.abstract N2 - The activity of tyrosine 3-monooxygenase in rat superior cervical ganglia in vitro was measured by monitoring their rate of dopa production. Cholinergic agonists produce a rapid and reversible increase in dopa synthesis in the ganglia. Carbachol (0.1 mM) causes a 5- to 6-fold increase in dopa synthesis. The action of carbachol is largely inhibited by the nicotinic antagonist hexamethonium (3 mM) and is completely blocked by a combination of hexamethonium and the muscarinic antagonist atropine (6 microM). Dimethylphenylpiperazinium (1 mM), a specific nicotinic agonist, produces a 4-fold increase in dopa synthesis. The action of dimethylphenylpiperazinium is blocked by hexamethonium but not by atropine. Bethanechol (1 mM), a muscarinic agonist, causes a 2-fold increase in dopa synthesis. The action of bethanechol is inhibited by atropine but not by hexamethonium. It is concluded that tyrosine 3-monooxygenase activity in rat superior cervical ganglia can be increased by both nicotinic and muscarinic stimulation, that nicotinic stimulation can produce a greater increase than can muscarinic stimulation and that carbachol increases enzyme activity by a combination of both pathways. These cholinergic mechanisms for the acute regulation of tyrosine 3-monooxygenase may be activated in vivo by acetylcholine released from preganglionic neurons and thus may play a role in the physiological regulation of catecholamine synthesis in sympathetic ganglia. ER -