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.
 ...
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

The interaction of (+)-amphetamine with haloperidol and gamma-butyrolactone on synthesis of monoamines in rat brain regions was investigated using an in vivo method, in which the accumulation of dopa and 5-hydroxytryptophan (5-HTP) was measured after inhibition of the aromatic amino acid decarboxylase by means of 3-hydroxybenzylhydrazine. The accumulation of 3-methoxytyramine (3-MT) after inhibition of the monoamine oxidase with pargyline was taken as an indicator of the in vivo release of dopamine (DA) into the extraneuronal space. (+)-Amphetamine at doses of 1--3 mg/kg caused an increase of dopa formation in the DA-rich areas c. striatum and mesolimbic forebrain but had no effect on dopa formation in neocortex and 5-HTP formation in all brain regions investigated. At a dose of 10 mg/kg (+)-amphetamine decreased dopa as well as 5-HTP formation in all brain regions studied. 3-MT accumulation in whole rat brain was stimulated by (+)-amphetamine as well as haloperidol and inhibited by gamma-butyrolactone. Combined treatment with haloperidol and (+)-amphetamine not only potentiated the stimulation of dopa formation but also the increase of 3-MT accumulation. Pretreatment with gamma-butyrolactone antagonized the stimulation of 3-MT formation induced by (+)-amphetamine at a dose of 10 mg/kg. This dose of (+)-amphetamine markedly counteracted the gamma-butyrolactone-induced increase in dopa formation especially in the DA-rich areas. The data support the view that impulse flow in DA neurons facilitates the effect of (+)-amphetamine on DA release and DA synthesis. Inhibition of catecholamine synthesis after high doses of (+)-amphetamine may be due to an increase in cytoplasmatic DA concentration causing end-product inhibition of tyrosine hydroxylase.
 ...
PMID:Interaction of haloperidol and gamma-butyrolactone with (+)-amphetamine-induced changes in monoamine synthesis and metabolism in rat brain. 32 21

1 The concentrations of p- and m-tyramine, dopamine and homovanillic acid were measured in the mouse striatum following the subcutaneous administration of amfonelic acid, (+)-amphetamine or nomifensine.2 The administration of 2.5-25 mg/kg of amfonelic acid produced a reduction in p-tyramine that lasted at least 8 h. m-Tyramine was significantly increased and this was observed between 2 and 24 h after drug treatment. The levels of homovanillic acid were increased within 4 h after amfonelic acid administration.3 (+)-Amphetamine treatment (5 mg/kg) produced a reduction in p-tyramine observed up to 4 h after its administration and no significant changes in m-tyramine.4 The administration of 10 mg/kg of nomifensine produced no significant changes in p-tyramine, m-tyramine or homovanillic acid. By increasing the dose to 20 mg/kg, nomifensine produced an increase in p-tyramine and homovanillic acid.5 The present results support the view that amfonelic acid and (+)-amphetamine would respectively release granular or newly synthesized dopamine, both actions being accompanied by an increase in tyrosine hydroxylase activity and dopamine turnover which in turn reduces p-tyramine but produces no change or an increase in m-tyramine.6 The effects of nomifensine were observed after the administration of a relatively high dose (20 mg/kg), that was lethal to some mice (about 20%, at 2 h), and more likely to posses unspecific actions.
 ...
PMID:The effects of amfonelic acid and some other central stimulants on mouse striatal tyramine, dopamine and homovanillic acid. 713