Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In the long-term ovariectomized rat the secretion of LH has a pulsatile character. In such rats no difference was observed between morning and afternoon LH secretion. The administration of phenoxybenzamine, an chi-adrenergic blocker, resulted in depressed plasma LH levels. chi-Methyl-tyrosine (chi-MT), an inhibitor of tyrosine hydroxylase had no effect on plasma LH levels, whereas bis(4methyl-1-homopiperazinil-thiocarbonil) disulphide (FLA 63), an inhibitor of dopaminic-beta-hydroxylase, induced decreased plasma LH levels and disappearance of the pulsations. The same effect was observed after the administration of apomorphine, a dopaminic receptor stimulating drug, whereas the administration of 1-hydroxy-3-amino-pyrrolidone-2 (HA-966), which blocks dopamine release, significantly raised plasma LH levels. Scopolamine, a cholinergic muscarinic receptor blocking drug, had no effect on plasma LH levels, whereas mecamylamine, a cholinergic nicotine receptor blocking agent, decreased them. These results are consistent with the hypothesis that the pulsatile release of LH in the long-term ovariectomized rat is caused by the stimulating activity of adrenergic and cholinergic, probably nicotinic, systems and the inhibitory activity of a dopaminergic system.
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PMID:Involvement of catecholaminergic and cholinergic mechanisms in the pulsatile release of LH in the long-term ovariectomized rat. 0 41

Cortical choline acetyltransferase (ChAT), tyrosine hydroxylase (TH), tryptophan hydroxylase (TPH), muscarinic receptors and sodium-dependent, high-affinity, choline uptake (SDHACU) sites were examined in the rat brain following unilateral stereotaxic injection of the cholinotoxin, AF64A, into the nucleus basalis magnocellularis (NBM). Injection of AF64A resulted in a significant loss of presynaptic cholinergic markers in the cortex without alteration in TH and TPH activity. The binding to SDHACU sites was reduced to background values in the NBM and increased in the central amygdala (Ce) and cortex. The increase in cortical [3H]QNB binding was the result of a change in muscarinic receptor number (BMAX) and not a change in receptor affinity (KD). Examination of muscarinic receptor subtypes demonstrated a reduction of M1 receptor binding in the cortex and NBM without any alteration in the Ce. Non-M1 binding was significantly increased in all the laminae of the cortex and in the Ce, but decreased in the NBM. These data suggest that there exists a population of M1 receptors on NBM projections to the cortex and that NBM projections influence a population of postsynaptic receptors in the cortex and Ce which are not of the M1 subtype.
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PMID:Alterations in cortical muscarinic receptors following cholinotoxin (AF64A) lesion of the rat nucleus basalis magnocellularis. 134 2

Grafts of fetal striatum were implanted in the form of a cell suspension into the brains of rats with prior ibotenic acid lesions of the caudate-putamen. The grafts were placed in three different sites: the lesioned caudate-putamen, or the denervated (but otherwise undamaged) globus pallidus and substantia nigra. After 3-6 months survival the grafts were investigated by means of immunohistochemistry and receptor autoradiography in combination with routine histology and acetylcholinesterase histochemistry. The grafts placed within the lesioned caudate-putamen were at least 10-fold larger larger than those placed in the substantia nigra region, with the grafts placed in the globus pallidus being of intermediate size. In all locations the acetylcholinesterase staining had an uneven, patchy distribution, which was most pronounced in the grafts located within the caudate-putamen. These patches did not bear any obvious relationship to variations in density of the neuronal perikarya within the grafted tissue. Many of the neuropeptide-immunoreactive neuron types present in the normal striatum, such as those containing substance P, [Met]enkephalin, somatostatin, cholecystokinin and neuropeptide Y were also detected in the grafted striatum along with acetylcholinesterase-positive staining. Acetylcholinesterase-positive, [Met]enkephalin-positive, substance P-positive and tyrosine hydroxylase-positive markers all showed uneven, patchy distributions in the grafts. This was also the case for the distribution of dopamine D2 and opiate receptors (as revealed by [3H]spiroperidol and [3H]diprenorphine autoradiography, respectively), whereas muscarinic receptor binding was even throughout the grafts. As is the case in the so-called striosomal patches (neurochemically defined compartments) in the immature intact striatum during the early postnatal period, patches of high acetylcholinesterase staining in the grafts showed partial correspondence with patches of high [Met]enkephalin fibre staining, and dopamine receptor density, and (although to a lesser degree) also with patches of high opiate receptor density and high substance P-immunoreactivity. This correspondence of patches also occurred between tyrosine hydroxylase fibre staining and acetylcholinesterase staining as revealed by grafts placed into the substantia nigra. These results suggest that the fetal striatal cell suspension grafts will give rise to a fairly normal range of striatal neuron and receptor types and that they develop at least some of the striosomal features characteristic for the normal striatum.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neural grafting in a rat model of Huntington's disease: striosomal-like organization of striatal grafts as revealed by acetylcholinesterase histochemistry, immunocytochemistry and receptor autoradiography. 282 74

Autoradiographic examination of the response of muscarinic cholinergic (M1 and M2) receptors to multiple doses of methamphetamine has been performed in several regions of the rat brain. Both muscarinic receptor subtypes were identified with [3H]-N-methylscopolamine, while M1 receptors were specifically labeled with [3H]-pirenzepine. No change in muscarinic receptors labeled with [3H]-pirenzepine was found in any of the brain regions examined following methamphetamine treatment; however, [3H]-N-methylscopolamine binding was significantly reduced (24-40%). These results indicate that M1 receptors remained unchanged after the drug treatment, while M2 receptors were reduced in many areas of the rat central nervous system following multiple high doses of methamphetamine. Five doses of methamphetamine (6-hour interval between doses) were required to elicit the receptor changes in all brain regions analyzed. Within 7 days after drug treatment, the receptor number returned to control values in the affected brain areas. Additionally, the response of serotonin (5-HT1 and 5-HT2) receptors to methamphetamine was examined and found to be reduced in a few brain areas analyzed. The receptor changes were accompanied by METH-induced decreases in tyrosine hydroxylase and tryptophan hydroxylase activities.
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PMID:Autoradiographic analysis of muscarinic cholinergic and serotonergic receptor alterations following methamphetamine treatment. 289 16

Administration of 6-hydroxydopamine to adult rats results in changes in the superior cervical ganglion similar to those noted after axotomy; namely, a decrease in muscarinic receptor binding and increases in activities of the oxidative enzymes of the pentose phosphate pathway. These changes were either prevented or attenuated markedly by the systemic administration of nerve growth factor. Administration of nerve growth factor alone did not significantly increase N-methylscopolamine binding in the ganglion or reduce the activities of the oxidative enzymes. Explants of the ganglion maintained in serum-free medium over a period of 3 days demonstrated increases in oxidative enzyme activity and a decrease in N-methylscopolamine binding. Addition of 20 nM nerve growth factor to the culture medium prevented the decline in N-methylscopolamine binding in ganglion explants. The increases in oxidative enzyme activities were unaltered. Addition of high amounts of nerve growth factor, 200 nM, resulted in a significant increase in tyrosine hydroxylase activity but no further increase in N-methylscopolamine binding in ganglion explants. Glucocorticoids added to the culture medium did not affect the muscarinic binding or enzyme activities. Thus, decreases in muscarinic binding activity which occur in the superior cervical ganglion after axotomy or 6-hydroxydopamine treatment may be explained by a loss of nerve growth factor supplied to the ganglion. Increases in the oxidative enzymes of the pentose phosphate pathway that occur in the ganglion after axonal injury appear to involve additional factors.
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PMID:Muscarinic receptor binding and oxidative enzyme activities in the adult rat superior cervical ganglion: effects of 6-hydroxydopamine and nerve growth factor. 613 21

Two strains of Mus musculus musculus, C57BL/6J and CD-1, and Mus musculus poschiavinus, the tobacco mouse, were used to study the effects of increased gene dosage of mouse chromosome 16 (MMU 16). A developmental delay has been found in the brains of murine trisomy 16 (Ts16) fetuses. Both the brain weight (in all three strains) and DNA content (in CD-1) were reduced, while protein content was unchanged in Ts16 compared to normal littermates. The daily increments of weight and protein (except in M. m. poschiavinus) were significantly greater in Ts16. The activities of choline acetyltransferase and acetylcholinesterase and muscarinic receptor binding were reduced. Their daily increments were also reduced to less than 56% that of littermates in Ts16 brains. The rate limiting enzymes of catecholaminergic neurons, tyrosine hydroxylase and dopamine beta-hydroxylase, and the concentration of catecholamines in the brains of Ts16 animals were lower. The activities of three other catecholaminergic enzymes, DOPA decarboxylase, catechol O-methyltransferase, and monoamine oxidase, were generally elevated in Ts16 brain, as were their daily increments. These observations indicate a significant developmental alteration in the maturation of the trisomic brain and suggest future avenues for defining the effect of increased gene dosage of MMU 16 in the CNS.
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PMID:Neurochemical changes in murine trisomy 16: delay in cholinergic and catecholaminergic systems. 614 55

We investigated transcriptional regulation of the rat tyrosine hydroxylase (TH) gene by muscarinic stimulation in human neuroblastoma SK-N-BE(2)M17 cells. Carbachol treatment increased the levels of intracellular Ca2+ and inositol 1,4,5-trisphosphate (IP3) and enhanced transcription of the TH gene. The muscarinic receptor antagonist atropine completely abolished the carbachol effect on TH gene expression. When cells were loaded with 50 microM 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester (BAPTA/AM) to chelate intracellular Ca2+, carbachol still raised intracellular IP3 level and enhanced TH gene expression. Transient transfection analysis of the 5' upstream region of TH gene revealed that the AP1 cis-acting element at -205 to -199 bp was responsible for carbachol stimulation. But carbachol did not enhance TH gene expression in protein kinase C (PKC)-activated or down-regulated cells that had been induced by 5-min or 24-h exposure to phorbol 12-myristate 13-acetate (PMA), respectively. Thus, Ca(2+)-independent PKC may play a role in carbachol-induced TH gene expression. We demonstrated by gel retardation and competition assays that a DNA sequence containing the wild-type AP1 site formed the specific DNA-protein complex. However, treatment with carbachol or PMA did not change the amount of the specific DNA-protein complex. Our results indicate that stimulation of phospholipase C-linked muscarinic receptors leads to elevated TH gene expression via AP1-mediated enhancement in a PKC-dependent pathway.
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PMID:AP1-mediated transcriptional enhancement of the rat tyrosine hydroxylase gene by muscarinic stimulation. 876 93

Catecholamines (CA) were studied in peripheral human lymphocytes in basal conditions as well as after L-tyrosine and/or acetylcholine (ACh) stimulation. Nicotinic and muscarinic receptor activation and blockade were assessed. CA were determined after ultrasonic cell disruption in peripheral lymphocytes after incubation (1 h at 37 degrees C) with the chemicals employed. L-tyrosine significantly increased (P < 0.01) L-Dopa and norepinephrine (NE) content of lymphocytes. ACh in the low microM range did not modify, whereas ACh (60 microM) and (120 microM) significantly increased (P < 0.01), both L-Dopa and NE intracellular levels. L-tyrosine plus ACh (60 microM) or (120 microM) significantly increased (P < 0.01) intracellular L-Dopa and NE versus control, versus L-tyrosine alone and versus ACh alone. The increase was higher than the algebraic sum of the individual increases. Nicotine (250 microM), but not muscarine (50 microM), significantly increased L-Dopa and NE in lymphocytes. Tetraethylammonium (500 microM) (nicotinic blocker), but not atropine (100 microM) (muscarinic blocker), inhibited the ACh-mediated increase of intracellular L-Dopa and NE. These data show that lymphocyte synthesis of CA is under nicotinic control. Since intracellular L-Dopa after L-tyrosine plus ACh increased 6-fold versus basal, 2-fold versus L-tyrosine alone and 3-fold versus ACh alone, it is concluded that ACh might regulate CA synthesis in lymphocytes through an activation of the rate limiting enzyme tyrosine hydroxylase.
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PMID:L-tyrosine and nicotine induce synthesis of L-Dopa and norepinephrine in human lymphocytes. 911 63

Regulation of tyrosine hydroxylase (TH) enzymatic activity in vivo by muscarinic receptor agonists in rat adrenal medulla was characterized in this study. Bethanechol and carbachol produce dose-dependent increases in rat adrenal TH activity. These increases are maximal (approximately 3-fold) using 10 mg/kg bethanechol or 0. 5 mg/kg carbachol and are totally inhibited by prior administration of 2 mg/kg atropine but not by 15 mg/kg hexamethonium. Transection of the splanchnic nerve innervating the adrenal gland leads to a loss in the activation of TH elicited by bethanechol, suggesting that transsynaptic influences are necessary for enzyme activation. When bethanechol is administered repeatedly once every hour for 3 hr (four injections), TH activity is not increased 20 min after the last injection, suggesting that the muscarinic receptor-mediated response desensitizes. In contrast, when nicotine is administered repeatedly once every hour for 3 hr, TH remains activated 20 min after the last injection. Cross-tolerance between the nicotine- and bethanechol-mediated effects on TH enzyme activity are not observed, when rats are injected repeatedly with nicotine and then administered bethanechol or vice versa. Coadministration of atropine and hexamethonium does not inhibit the nicotine-mediated activation of TH, suggesting that noncholinergic receptors participate in the transsynaptic activation of adrenal TH elicited by nicotine. Our results demonstrate that agonist occupation of muscarinic cholinergic receptors is associated with activation of TH enzyme in rat adrenal medulla. However, stimulation of the adrenal muscarinic receptor is not essential for the transsynaptic regulation of the enzyme.
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PMID:Regulation of tyrosine hydroxylase activity by muscarinic agonists in rat adrenal medulla. 969 41

The neurochemical profile was examined at postnatal day 3-4 in mutant mice generated by in vivo Cre mediated activation of an attenuated diphtheria toxin gene inserted into the D1 dopamine receptor gene locus. An earlier study of this model had shown that D1 dopamine receptor, substance P and dynorphin were not expressed in the striatum. Quantitative in situ hybridization analysis showed an increase in D2 dopamine receptor and enkephalin messenger RNA expression. The nigrostriatal pathway in the mutant pups was intact with a normal number of dopaminergic neurons in the substantia nigra and the ventral tegmental area in addition to a normal pattern of striatal dopamine transporter and tyrosine hydroxylase immunoreactivity. Quantitative analysis of striatal dopamine transporter density using [3H]mazindol showed a reduction of 26% suggesting a degree of transneuronal down-regulation. There was also a 49% reduction of striatal GABA receptor binding and a 36% reduction of striatal muscarinic receptor binding in mutant pups. The number of healthy striatal neuropeptide Y-containing interneurons was also substantially down-regulated in the mutant striatum. In contrast, there was an increase in the number of striatal cholinergic interneurons. Down-regulated cortical GABA receptor and muscarinic receptor binding was also observed in addition to subtle morphological changes in the neuropeptide Y-expressing population of cortical neurons. The changes reflect the early cascade of events which follows the ablation of D1 dopamine receptor-positive cells. Although extensive changes in a number of striatal and cortical neurons were demonstrated, only subtle transneuronal effects were seen in the nigrostriatal pathway.
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PMID:Early direct and transneuronal effects in mice with targeted expression of a toxin gene to D1 dopamine receptor neurons. 1068 9


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