Selective response of rat peripheral sympathetic nervous system to various stimuli.
1. We utilized the induction of tyrosine hydroxylase, a catecholamine-synthesizing enzyme, in sympathetic ganglia and adrenal medullae to explore the central and peripheral mechanisms through which choline, various environmental stresses, and drugs that alter blood pressure or central neurotransmission affect various portions of the sympathetic nervous system. Animals received each treatment chronically, and enzyme activity was measured in the superior cervical, stellate, and coeliac ganglia and in the adrenal medullae.2. Choline administration increased tyrosine hydroxylase activity in all four tissues, probably by increasing the release of acetylcholine from preganglionic sympathetic neurones that synapse on catecholamine-producing ganglion and chromaffin cells; carbachol and nicotine had similar effects.3. Insulin enhanced tyrosine hydroxylase activity primarily in the coeliac ganglion and the adrenal medullae, but not in the superior cervical ganglia.4. Reserpine and phenoxybenzamine increased the activity of the enzyme in all four tissues.5. Prolonged exposure to a cold environment increased enzyme activity in all four tissues, but especially in the stellate and coeliac ganglia; forced swimming affected tyrosine hydroxylase only in these two ganglia.6. Several drugs known to modify central neurotransmission were found to increase tyrosine hydroxylase activity in some portions of the sympathetic nervous system but not in others. 5,7-Dihydroxytryptamine, which destroys terminals of serotoninergic neurones, enhanced enzyme activity in all four tissues, but primarily in the coeliac ganglion and adrenal medullae. ET-495 (a dopaminergic agonist), D-amphetamine, and morphine induced tyrosine hydroxylase activity in the adrenal medullae and the coeliac ganglion, but not in the superior cervical ganglia. Oxotremorine, a centrally acting muscarinic agonist, increased tyrosine hydroxylase activity only in the adrenal medullae; its effect was not blocked by methylatropine, a peripheral muscarinic blocker.7. These data indicate that specific neurones in the central nervous system, which utilize specific neurotransmitters and which are differentially affected by drugs and environmental inputs, selectively influence the outflows through the various zones of the sympathetic nervous system.
D015116:5,7-Dihydroxytryptamine / Q000494:pharmacology; D000313:Adrenal Medulla / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D000818:Animals; D002794:Choline / Q000494:pharmacology; D003080:Cold Temperature; D003913:Dextroamphetamine / Q000494:pharmacology; D005728:Ganglia, Sympathetic / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009020:Morphine / Q000494:pharmacology; D010095:Oxotremorine / Q000494:pharmacology; D010643:Phenoxybenzamine / Q000494:pharmacology; D051381:Rats; D012110:Reserpine / Q000494:pharmacology; D013312:Stress, Physiological / Q000503:physiopathology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D007328:Insulin; D010643:Phenoxybenzamine; D015116:5,7-Dihydroxytryptamine; D010095:Oxotremorine; D009020:Morphine; D012110:Reserpine; D014446:Tyrosine 3-Monooxygenase; D002794:Choline; D003913:Dextroamphetamine