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Selective response of rat peripheral sympathetic nervous system to various stimuli
Abstract:
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.
Insights
This study investigated how choline, stress, and drugs impact the sympathetic nervous system by measuring tyrosine hydroxylase activity. Findings reveal differential effects on various sympathetic regions, highlighting specific central nervous system control.
Area of Science:
- Neuroscience
- Pharmacology
- Physiology
Background:
- The sympathetic nervous system regulates physiological responses.
- Tyrosine hydroxylase (TH) is a key enzyme in catecholamine synthesis, making it a marker for sympathetic nervous system activity.
- Understanding how external factors influence sympathetic outflow is crucial for various medical conditions.
Purpose of the Study:
- To investigate the effects of choline, environmental stresses, and drugs on tyrosine hydroxylase activity in different parts of the sympathetic nervous system.
- To explore central and peripheral mechanisms influencing sympathetic nervous system function.
- To determine how specific neurotransmitters and external stimuli differentially affect sympathetic outflow.
Main Methods:
- Chronic administration of choline, insulin, reserpine, phenoxybenzamine, and various psychoactive drugs to animals.
- Exposure to environmental stressors like cold and forced swimming.
- Measurement of tyrosine hydroxylase enzyme activity in superior cervical, stellate, and coeliac ganglia, and adrenal medullae.
Main Results:
- Choline, carbachol, and nicotine increased TH activity in all tested tissues.
- Insulin primarily affected the coeliac ganglion and adrenal medullae.
- Reserpine and phenoxybenzamine increased TH activity across all tissues.
- Cold exposure and forced swimming elevated TH activity, with specific regional effects.
- Drugs modulating central neurotransmission showed differential impacts on TH activity in various sympathetic regions.
Conclusions:
- Central nervous system neurons, utilizing specific neurotransmitters, differentially regulate sympathetic nervous system outflow.
- Environmental factors and pharmacological agents can selectively influence distinct sympathetic pathways.
- The study provides insights into the complex, regionally specific control of the sympathetic nervous system.