Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Selective response of rat peripheral sympathetic nervous system to various stimuli. 4 Oct 93

In the rat, oxotremorine increases the threshold for vocalisation after-discharge (affective component of pain reactions) dose dependently at subtremor doses (30-67 mug/kg s.c.). Doses of 225-506 mug/kg were needed to elevate the thresholds for vocalisation and motor response. 1-Tryptophan, PCPA, alpha-methyl-p-tyrosine, 1-Dopa, pimozide and LSD-25 did not affect the antinociceptive activity of oxotremorine, while phenocybenzamine slightly increased the threshold for vocalisation. Oxotremorine did not change the endogenous brain concentrations of noradrenaline and dopamine or 5-HT but decreased that of 5-HIAA in all brain regions at the time of maximal analgesia. The decrease of 5-HIAA was still present after pretreatment with probenecid. After inhibition of tyrosine hydroxylase, oxotremorine accelerated the depletion of dopamine in telencephalic cortex during maximal antinociceptive activity and of noradrenaline in all brain regions at a time when this activity had vanished. Atropine significantly antagonized the analgesic activity of oxotremorine. It is concluded that oxotremorine antinociceptive activity in the rat is related to a cholinergic compoent, while a monoaminergic component is not directly involved.
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PMID:Antinociceptive action of oxotremorine and regional turnover of rat brain noradrenaline, dopamine and 5-HT. 23 55

Adult male Sprague-Dawley rats were given hourly injections of physostigmine for 1--4 h, and the effect of this treatment on dopamine (DA) and noradrenaline (NA) content or on DA and NA was estimated by measuring the decline in these amines produced following the inhibition of tyrosine hydroxylase with alpha-methyl-p-tyrosine (alpha MPT). In later experiments oxotremorine was administered instead of physostigmine at hourly intervals for 2 h. Physostigmine administration resulted in a highly significant increase in the depletion of NA produced by alpha MPT indicating that the turnover of NA was increased by this drug. This effect was observed in the medial basal hypothalamus and anterior hypothalamus but not in the telencephalon-thalamus. Oxotremorine also produced an increase in NA turnover, but this drug was effective in all three brain areas. Atropine pretreatment blocked the effect of both physostigmine and oxotremorine on NA turnover. However, in the case of physostigmine, atropine was only effective if it was given 30 min before each injection of physostigmine. Mecamylamine, a nicotine blocker, did not reverse the effect of physostigmine on NA turnover. These results suggest that there is a cholinergic input via muscarinic receptors which influences the activity of noradrenergic pathways terminating in the anterior or medial basal hypothalamus.
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PMID:Evidence for a cholinergic influence on catecholaminergic pathways terminating in the anterior and medial basal hypothalamus. 48 84

Marked enhancement of tyrosine hydroxylase (TH) activity was observed in the rostral pons of Wistar albino rats, 3 days after a single injection of Oxotremorine. TH activity in other brain areas, and regional levels of norepinephrine, dopamine, serotonin and 5-hydroxyindoleacetic acid were unaffected. Enhancement of TH activity did not affect length or number of REM episodes, or the amount of REM occurring in 24 hr. REM occurrence did not, thus, vary in accordance with activity of the rate-limiting enzyme for catecholamine synthesis. These data suggest that, although REM may reflect neuronal protein synthesis, REM is not part of a mechanism regulating the activity of enzymes in the pontine CA synthesis pathway.
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PMID:Enhancement of tyrosine hydroxylase activity by Oxotremorine does not affect sleep in the rat. 610 19

Differential pulse voltammetry with treated carbon fibre electrodes was used to study the effect of cholinergic drugs on the metabolism of locus coeruleus (LC) noradrenergic cells in vivo. A catechol peak corresponding to DOPAC synthesized by noradrenergic cells and reflecting their metabolic activity, was recorded every two minutes in the LC of freely moving rats. Cholinergic agonists like eserine (0.5 mg/kg s.c.) and oxotremorine (0.1 and 0.4 mg/kg s.c.) increased the DOPAC peak. This effect seemed to be mediated by muscarinic receptors since it was antagonized by scopolamine (5 mg/kg i.p.). Oxotremorine in high doses (1.5 mg/kg s.c. for 3 days) induced 'delayed activation' of tyrosine hydroxylase (+273%). In these conditions LC cells were no longer responsive to a challenge dose of oxotremorine though they maintained normal responsiveness to noradrenergic drugs. The results show that cholinergic drugs can greatly influence the metabolism of LC noradrenergic neurons.
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PMID:Cholinergic control of catechol metabolism in the rat locus coeruleus as studied by in vivo voltammetry. 614 45