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

An in vitro study was made of the influence of the atypical neuroleptics sulpiride and carbidine on the activity of synaptosomal tyrosine hydroxylase (TH) of the rat brain striatum. Dopamine was applied as an inhibitor of tyrosine hydroxylation (10(-6) M), dopamine uptake was blocked by nomifensine (10(-5) M). The experiments were performed in two versions: in a medium containing common (5 mM) and depolarizing concentration of potassium ions. In both the cases sulpiride did not exert any noticeable effect on TH activity but significantly lowered the inhibitory action of dopamine. In a medium containing 30 mM potassium, carbidise inhibited the rate of TH hydroxylation and enhanced the inhibitory action of dopamine on TH activity under blockade of its uptake by nomifensine. It is assumed that the mechanisms of the action of carbidine and sulpiride are different.
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PMID:[Effect of the atypical neuroleptics karbidin and sulpiride on the synaptosomal tyrosine hydroxylase of the corpus striatum of rats]. 614 73

Neurons containing the enzyme aromatic L-amino acid decarboxylase were immunocytochemically localized in the brain stem of the rat. The enzyme occurred as expected in previously well characterized monoaminergic cell groups, and in addition in some nuclei with unknown neurotransmitters. Major aggregates of neurons that were immunoreactive for aromatic L-amino acid decarboxylase but contained neither tyrosine hydroxylase nor serotonin, were found in the pretectal nuclei, the lateral parabrachial nucleus, and the dorsolateral subdivision of the nucleus tractus solitarius. Aromatic L-amino acid decarboxylase was also present in serotonin neurons and the majority of catecholamine cell groups. Dopamine, noradrenaline, and adrenaline cells exhibited characteristic staining intensities to anti-aromatic L-amino acid decarboxylase reflective of relative enzyme levels in the different groups. Some cells in the dorsal motor nucleus of the vagus that were previously classified as dopaminergic lacked immunoreactivity to aromatic L-amino acid decarboxylase.
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PMID:Aromatic L-amino acid decarboxylase in the rat brain: immunocytochemical localization in neurons of the brain stem. 637 83

The presence of enzymatic activity (tyrosine hydroxylase, dopa-decarboxylase, dopamine-beta-hydroxylase, monoamine oxydase and catechol-O-methyl transferase), as well as dopamine (DA) content and DA synthesis from tyrosine and dopa, were investigated in intact rats partes distales and in grafts (both estrogenized and nonestrogenized). Counts of prolactin cells showed the following regression in the number of these cells: estrogenized grafts greater than nonestrogenized grafts greater than intrasellar intact glands. Tyrosine hydroxylase activity was not found in intact glands, but this enzyme was detected in the two types of grafts. An approximate correlation could be established between the number of prolactin cells and the diverse enzyme activities. Dopamine was not synthesized from tyrosine in intact glands, but it occurred in the transplants. However, when dopa was used, both intact and grafted glands produced dopamine. Estrogen administration decreased dopamine content in all the glands investigated. The significance of these results in relation to the physiology of the pars distalis is discussed.
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PMID:Catecholamine metabolizing enzymes and synthesis of dopamine in normal and grafted pituitary partes distales. 664 50

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 catecholamine (CA) content was measured in nerve terminals of the median eminence (ME) in normal, castrated and adrenalectomized male rats using quantitative microfluorimetry. CA turnover was determined by rates of CA disappearance after tyrosine hydroxylase inhibition. Noradrenaline (NA) levels and turnover in the subependymal layer (SEL) were unchanged 4 weeks after respective surgeries. Dopamine (DA) levels but not turnover in the lateral palisade zone (LPZ) were increased by castration. DA levels and turnover rates were significantly increased in the medial palisade zone (MPZ) by castration, whereas adrenalectomy selectively decreased MPZ CA levels without affecting the turnover rates. These results were discussed in relation to the concept of a medial and a lateral tuberoinfundibular DA pathway innervating different neuroendocrine structures in the rat ME.
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PMID:Increase in medial palisade zone dopamine activity after long-term castration in the male rat. 747 Feb 51

Rat brain catecholamine metabolism was changed over a period of several days by limited access to water (10 min/day). One or two weeks limited access to water caused an increase in hypothalamic norepinephrine metabolism as measured with alpha-methyl-para-tyrosine. Brain stem and telencephalon norepinephrine was not affected by the limited access to water regimen. Dopamine metabolism in the corpus striatum and the hypothalamus was not altered by limited access to water. If the limited access to water was continued for 3 or more weeks, hypothalamic norepinephrine metabolism then returned to normal. The increase in hypothalamic norepinephrine metabolism was confirmed by a second method measuring in vivo tyrosine hydroxylase activity. Additional experiments demonstrate that this affect is specific for water deficits. Limited access to food had no effect on the metabolism of norepinephrine in the hypothalamus. Water deficits produced by replacing water with a 2% NaCl solution caused a similar increase in hypothalamic norepinephrine metabolism to that observed after one week limited access to water. Furthermore, 10 min access to water stopped the increased hypothalamic metabolism of norepinephrine seen after one week of limited access to water. The regional specificity (effect seen in hypothalamus but not the telencephalon and brain stem), and the stimulus specificity (water and not food deficits) suggest hypothalamic norepinephrine involvement in thirst or hormonal control of water regulation.
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PMID:Increased hypothalamic norepinephrine metabolism after water deprivation in the rat. 747 Sep 17

We have examined several aspects of neurotransmitter function in the brains of mice carrying a deletion mutation in the gene encoding the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT). During the first 6 weeks of postnatal development, dopamine levels in whole-brain extracts from the mutant mice (HPRT-) failed to increase at rates comparable to normal animals, resulting in 40% lower dopamine levels throughout adulthood. Regional analysis in adult animals showed the caudoputamen to be the most severely affected region, with dopamine deficits of 48-64%. Dopamine levels in other regions were normal or less severely affected. The decrease in dopamine was accompanied by a decrease in tyrosine hydroxylase (TH) activity, the rate-limiting step in dopamine synthesis. Kinetic analysis of TH extracted from the caudoputamen of normal and HPRT- mice demonstrated a 45% decrease in Vmax with an increased affinity for the tetrahydropterin cofactor in the mutants. Labeling of midbrain dopamine neurons using TH immunohistochemistry revealed no obvious deficits in the number of midbrain dopamine neurons, but quantitative autoradiographic studies revealed significant reductions in the binding of 3H-N-[1-(2-benzo(beta)thiophenyl)cyclohexyl]piperidine (3H-BTCP) to dopamine uptake sites in the forebrain of the mutants. In contrast to these abnormalities of the dopamine systems in the mutant mice, other neurotransmitter systems appeared relatively unaffected. Norepinephrine, 5-HT, tryptophan hydroxylase, and glutamic acid decarboxylase were present at normal levels in the brains of the mutants. ChAT activity was slightly lower than normal in the caudoputamen of the mutant animals, but was normal in all other brain regions examined. These results indicate that HPRT deficiency is associated with a relatively specific deficit in basal ganglia dopamine systems that emerges during the first 2 months of postnatal development.
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PMID:Dopamine deficiency in a genetic mouse model of Lesch-Nyhan disease. 750 65

The distribution of dopaminergic fibers in the principal components of the central extended amygdala (central amygdaloid nucleus (Ce), substantia innominata, and bed nucleus of the stria terminalis (BNST)), was studied using immunocytochemistry against tyrosine hydroxylase, dopamine beta-hydroxylase and dopamine. Dopamine fibers were found most densely distributed in the dorsolateral subdivision of the BNST and the lateral part of the Ce. Smaller numbers of dopaminergic fibers were found in the rest of the central extended amygdala. In contrast, dopamine beta-hydroxylase fibers were virtually absent from the dorsolateral bed nucleus of the stria terminalis and lateral part of the central amygdaloid nucleus, but were distributed in a moderate density in the medial part of Ce, dorsal substantia innominata and posterolateral BNST. Our results show that dopamine fibers are most concentration over those regions of the central extended amygdala with large numbers of GABAergic neurons whose projections remain within the central extended amygdala, while noradrenergic fibers are most heavily concentrated over those regions containing a large proportion of brainstem projection neurons. That dopamine fibers are concentrated over regions with GABAergic medium spiny neurons suggests that those regions might be organized as a striatal parallel.
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PMID:Distribution of dopaminergic fibers in the central division of the extended amygdala of the rat. 751 Oct 34

The amphibian Xenopus laevis is able to adapt the colour of its skin to the light intensity of the background, by releasing alpha-melanophore-stimulating hormone from the pars intermedia of the hypophysis. In this control various inhibitory (dopamine, gamma-aminobutyric acid, neuropeptide Y, noradrenaline) and stimulatory (thyrotropin-releasing hormone and corticotropin-releasing hormone) neural factors are involved. Dopamine, gamma-aminobutyric acid and neuropeptide Y are present in suprachiasmatic neurons and co-exist in synaptic contacts on the melanotrope cells in the pars intermedia, whereas noradrenaline occurs in the locus coeruleus and noradrenaline-containing fibres innervate the pars intermedia. Thyrotropin-releasing hormone and corticotropin-releasing hormone occur in axon terminals in the pars nervosa. In the present study, the neuronal origins of these factors have been identified using axonal tract tracing. Application of the tracers 1,1'dioctadecyl-3,3,3',3' tetramethyl indocarbocyanine and horseradish peroxidase into the pars intermedia resulted in labelled neurons in two brain areas, which were immunocytochemically identified as the suprachiasmatic nucleus and the locus coeruleus, indicating that these areas are involved in neural inhibition of the melanotrope cells. Thyrotropin-releasing hormone and corticotropin-releasing hormone were demonstrated immunocytochemically in the magnocellular nucleus. This area appeared to be labelled upon tracer application into the pars nervosa. This finding is in line with the idea that corticotropin-releasing hormone and thyrotropin-releasing hormone stimulate melanotrope cell activity after diffusion from the neural lobe to the pars intermedia. After anterograde filling of the optic nerve with horseradish peroxidase, labelled axons were traced up to the suprachiasmatic area where they showed to be in contact with suprachiasmatic neurons. These neurons showed a positive reaction with anti-neuropeptide Y and the same held for staining with anti-tyrosine hydroxylase. It is suggested that a retino-suprachiasmatic pathway is involved in the control of the melanotrope cells during the process of background adaptation.
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PMID:Involvement of retinohypothalamic input, suprachiasmatic nucleus, magnocellular nucleus and locus coeruleus in control of melanotrope cells of Xenopus laevis: a retrograde and anterograde tracing study. 752 68

Neurodevelopmental and neurodegenerative disorders related to dopaminergic transmission typically exhibit a sex-specific prevalence. In order to investigate the underlying cellular mechanisms, primary cultures of dissociated embryonic rat midbrain were subject to a 24 h treatment with dopamine in concentrations between 1 and 1000 microM. Dopamine caused a dose-dependent loss of neurons and reduction of neurites immunoreactive to tyrosine hydroxylase with a LD50 of about 100 microM. Application of D1-like or D2-like receptor agonists instead of dopamine did not induce cell loss. Neither D1-like or D2-like receptor antagonists nor the nitric oxide synthase inhibitor N-nitro-L-arginine were capable of blocking dopamine-induced cell death. When tissue from male and female donors was cultured separately, a twofold sex difference was consistently present: (1) Survival rates of female dopaminergic neurons in the presence of LD50 concentrations of dopamine were about twice those of male neurons. (2) The N-methyl-D-aspartate-receptor antagonist AP-5 was capable of rescuing female but not male dopaminergic neurons from dopamine-induced cell death. It is concluded that dopamine neurotoxicity is not mediated by dopamine receptors and is aggravated by glutamate excitotoxicity but not by nitric oxide. The male-specific vulnerability is the first direct evidence that the prevalence of certain neurodevelopmental or neurodegenerative disorders may have a basis in the biology of the single dopaminergic neuron.
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PMID:Neurotoxicity of dopamine and protective effects of the NMDA receptor antagonist AP-5 differ between male and female dopaminergic neurons. 755 42


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