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)

Rats were kept on a 12-h light-dark cycle. One hour after the light was switched on, physiological saline, (+)-amphetamine 1 mg/kg, and H 77/77 5 mg/kg were injected s.c.; the number of groomings was counted 1-2 h after the treatments. (+)-Amphetamine and H 77/77 produced increased grooming which was antagonized by the tyrosine hydroxylase inhibitor H 44/68 (250 mg/kg), the dopamine-beta-hydroxylase inhibitor FLA 63 (40), the neuroleptics haloperidol (0.1 and 0.5), and clozapine (1 and 5). The (+)-amphetamine-induced grooming was also antagonized by the NA-receptor blocker aceperone (10) but not by the sedative phenothiazines mepazine (10) and diphenhydramine (20) nor diazepam (1). These results indicate that NA-release is involved in the mediation of (+)-amphetamine- and H 77/77-induced grooming. The inhibition of haloperidol and clozapine is presumably due to NA-receptor blockade.
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PMID:Evidence for a noradrenergic mechanism in the grooming produced by (+)-amphetamine and 4, alpha-dimethyl-m-tyramine (H 77/77) in rats. 14 28

Quantitative microfluorimetric studies were carried out on the formaldehyde induced fluorescence of dopamine in nerve terminals of the nuc. caudatus putamen using the technique of Falck and Hillarp. After tyrosine hydroxylase inhibition produced by alpha-methyl-p-tyrosine (H 44/68) a time-dependent disappearance of the dopamine fluorescence occurred in an exponential manner, T1/22.6 hr. Apomorphine treatment resulted in a considerable counteraction of the H 44/68 induced reduction of the fluorescence, whereas treatment with haloperidol potentiated it. Administration of gamma-hydroxybutyrolactone led to a marked increase of the dopamine fluorescene. The present microfluorimetric results were in perfect agreement with chemical-analytical determinations of dopamine carried out under identical experimental conditions, and with those reported previously. The fluorescence intensities obtained in the nuc. caudatus putamen were found to be in the linear part of the dopamine fluorescence concentration relationship as observed in protein models. It may be concluded that by using microfluorimetric quantitation of the formaldehyde induced fluorescence in the nuc. caudatus putamen it is possible to obtain a reliable quantitation of the relative amount of dopamine in the dopamine nerve terminals.
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PMID:Quantitative microfluorimetry of formaldehyde induced fluorescence of dopamine in the caudate nucleus. 23 82

The ex vivo effects of the antipsychotic dopamine receptor antagonist remoxipride on dopamine and noradrenaline turnover in the rat brain have been compared. Remoxipride (5-125 mumol/kg intraperitoneally) produced large increases in striatal DOPAC and HVA concentrations with only maginal effects on striatal, hippocampal and hypothalamic MHPG concentrations. Both remoxipride (5.6 mumol/kg intraperitoneally) and haloperidol (0.23 mumol/kg intraperitoneally) increased the rate of striatal dopamine disappearance following inhibition of tyrosine hydroxylase by H 44/68 without corresponding effect on hypothalamic and frontal cortical noradrenaline disappearance. It is concluded that at doses of remoxipride producing compensatory increases in dopamine turnover, there is little or no effect on noradrenaline turnover, confirming the in vitro dopamine:noradrenaline selectivity of this compound.
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PMID:Comparison of the effects of the novel antipsychotic agent remoxipride on dopamine and noradrenaline turnover in the rat brain. 257 99

Subchronic (5 mg/kg SC, twice daily for 14 days) but not acute administration of the beta-2-adrenoceptor agonist salbutamol to rats caused a significant increase in the accumulation of 5-hydroxytryptophan in the limbic forebrain, the corpus striatum and the cerebral cortex when measured during 30 min after inhibition of L-amino acid decarboxylase by NSD 1015 (100 mg/kg IP). Simultaneously assayed tryptophan concentrations in the same brain regions were not affected. These results indicate an increase in the in vivo rate of tryptophan hydroxylation in the brain, produced by subchronic salbutamol administration. The effect of salbutamol treatment on brain catecholamine(CA) utilization was estimated by studying the disappearance of CA in the brain after inhibition of tyrosine hydroxylase by alpha-methyltyrosine methyl ester (H 44/68), 250 mg/kg IP, 3.5 h before sacrifice. Subchronically but not acutely administered salbutamol caused both a significant increase in endogenous noradrenaline (NA) levels and an increase NA utilization. Dopamine levels and turnover were, however, not altered by either acute or subchronic treatment. The activation, probably centrally elicited, of brain NA and 5-hydroxytryptamine systems by the subchronic salbutamol regimen supports the concept of beta-adrenoceptor mediated regulation of brain monoamine systems, and could contribute to the clinically reported antidepressant activity of beta-2-adrenoceptor agonists.
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PMID:Increased brain serotonergic and noradrenergic activity after repeated systemic administration of the beta-2 adrenoceptor agonist salbutamol, a putative antidepressant drug. 678 36

The effects of high repeated subcutaneous doses (4 X 2 mg/kg) of nicotine have been evaluated on dopamine (DA) and noradrenaline (NA) levels and turnover in the long-term castrated male rat using catecholamine (CA) fluorescence histochemistry in combination with quantitative microfluorometry. The CA turnover was evaluated by studying the decline of the CA stores following tyrosine hydroxylase inhibition using alpha-methyltyrosine methyl ester (H 44/68). In the same experiments trunk blood was collected for the determination of serum prolactin, LH, FSH and TSH levels using standard radioimmunoassay procedures. The nicotine treatment produced a significant depletion of CA stores and an increase of CA turnover in DA and NA nerve terminals of the median eminence and in peri- and paraventricular NA systems. These effects were significantly counteracted by pretreatment with mecamylamine. Nicotine significantly reduced serum prolactin and TSH levels, and after H 44/68 it also reduced LH and FSH serum levels. These actions were counteracted by mecamylamine pretreatment, except the effects on serum TSH levels after H 44/68, which were even enhanced by pretreatment with mecamylamine. Overall intraindividual correlations showed a significant correlation between reduced CA turnover in several hypothalamic areas and increased serum LH and FSH levels, increased NA turnover in the paraventricular hypothalamic nucleus and increased serum TSH levels, and reduced DA turnover in the median eminence and increased serum LH levels. It is suggested that in the castrated male rat nicotine can activate cholinergic nicotine-like receptors facilitating DA and NA turnover and release in various hypothalamic CA nerve terminal systems including those inhibiting the secretion of prolactin and LH (DA terminals in medial and lateral palisade zone, respectively) and facilitating secretion of TSH (NA terminals in the parvocellular part of the paraventricular hypothalamic nucleus).
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PMID:Involvement of cholinergic nicotine-like receptors as modulators of amine turnover in various types of hypothalamic dopamine and noradrenaline nerve terminal systems and of prolactin, LH, FSH and TSH secretion in the castrated male rat. 681 38