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  • Title: Both nicotinic and muscarinic agonists acutely increase tyrosine 3-monooxygenase activity in the superior cervical ganglion.
    Author: Ip NY, Perlman RL, Zigmond RE.
    Journal: J Pharmacol Exp Ther; 1982 Nov; 223(2):280-3. PubMed ID: 6127400.
    Abstract:
    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.
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