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)

We have previously described hypertrophy of neurons containing estrogen receptor mRNA in the infundibular nucleus of postmenopausal women. In the present investigation we identified peptide mRNAs in the hypertrophied neurons and determined whether postmenopausal neuronal hypertrophy was accompanied by changes in gene expression. In the first study in situ hybridization was performed on sections from hypothalami of postmenopausal women (n = 3) using synthetic 35S-labeled cDNA probes complementary to mRNAs encoding estrogen receptor, substance-P (SP), neurokinin-B (NKB), POMC, cholecystokinin, dynorphin, CRF, enkephalin, galanin, neuropeptide-Y, GH-releasing hormone, and tyrosine hydroxylase. Neuronal cross-sectional areas and cell densities were measured with the aid of a computer microscope system. Neurons labeled with the NKB and SP probes were comparable in size, morphology, and distribution to the hypertrophied neurons containing estrogen receptor mRNA. In contrast, neurons labeled with other cDNA probes were sparsely distributed (CRF and dynorphin), smaller in size (neuropeptide-Y, galanin, GH-releasing hormone, enkephalin, cholecystokinin, and POMC), or located anterior to the hypertrophied population (tyrosine hydroxylase). In the second study sections from hypothalami of premenopausal (n = 3) and postmenopausal (n = 3) women were incubated with cDNA probes complementary to SP or NKB mRNAs. The mean cross-sectional areas of postmenopausal infundibular neurons containing NKB and SP mRNAs increased to 194% and 176% of premenopausal values, respectively. The autoradiographic grain densities of infundibular neurons labeled with either probe were also significantly increased in the postmenopausal group. Finally, the numbers of labeled neurons/tissue increased 6-fold (SP) and 15-fold (NKB) in the postmenopausal infundibular nucleus. These data demonstrate that human menopause is associated with marked increases in hypothalamic NKB and SP gene expression. We propose that neurons containing estrogen receptor, SP, and NKB mRNAs participate in the hypothalamic circuitry regulating estrogen negative feedback in the human.
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PMID:Hypertrophy and increased gene expression of neurons containing neurokinin-B and substance-P messenger ribonucleic acids in the hypothalami of postmenopausal women. 170 31

Two experiments examined the role of the sympathetic nerves in estradiol-induced fat pad weight losses in ovariectomized (OVX) rats. Rats were OVX, and the retroperitoneal white adipose tissue (RWAT) was unilaterally denervated 4 wk later. After 14 days of treatment with estradiol benzoate (EB, 2 micrograms/day), the intact pads lost 23% more weight than the denervated pads. There was no effect of denervation on fat pad weight or on cytosol estrogen receptor concentration in RWAT in the animals treated with sesame oil vehicle. These data suggest that the sympathetic nerves play a role in estrogen-induced reductions in fat pad weight but not via changes in adipose tissue cytosol estrogen receptors. A second experiment examined whether estradiol-induced fat pad weight losses are accompanied by increased norepinephrine (NE) turnover, an index of sympathetic activity, in adipose tissue. Rats were OVX and treated with EB or sesame oil vehicle. NE turnover was assessed by measuring the decline of tissue NE over time after injection of alpha-methyl-p-tyrosine, an inhibitor of tyrosine hydroxylase activity and thus NE biosynthesis. NE turnover in RWAT, but not heart, was significantly greater in animals treated with EB, suggesting that estradiol decreases fat pad weight in part by increasing sympathetic nervous system activity. It is possible that estradiol acts in the brain to regulate the activity of the sympathetic nerves to white adipose tissue and peripherally to alter adipose tissue responsiveness to catecholamines.
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PMID:Role of sympathetic nerves in effects of estradiol on rat white adipose tissue. 199 27

We have recently shown that the dopamine-beta-hydroxylase inhibitor, U-14,624, decreases the concentration of cytosol estrogen receptors in the mediobasal hypothalamus (MBH) and anterior pituitary gland (AP) in ovariectomized rats, but that it also causes cell nuclear accumulation of estrogen receptors. We tried to determine if this is the mechanism by which other catecholaminergic inhibitors decrease the concentration of cytosol estrogen receptors in either the MBH or AP. The previously reported decrease in the concentration of cytosol estrogen receptors in AP by the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine was confirmed. Also, the decrease in the concentration of cytosol estrogen receptors in MBH after treatment with the dopamine-beta-hydroxylase inhibitors, diethyldithiocarbamate and FLA 63 was demonstrated. In no case was an increase in the concentration of nuclear estrogen receptor accumulation detected after treatment with the drugs. Results of assays of norepinephrine and dopamine levels in MBH after the various treatments suggest that, at the dosage used, U-14,624 has a greater effect on norepinephrine and dopamine levels that the other dopamine-beta-hydroxylase inhibitors. The results of these experiments suggest that inhibitors of dopamine-beta-hydroxylase and tyrosine hydroxylase cause decreases in the concentration of cytosol estrogen receptors in either the MBH or AP that are not referable to increased cell nuclear accumulation of estrogen receptors.
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PMID:Some catecholamine inhibitors do not cause accumulation of nuclear estrogen receptors in rat hypothalamus and anterior pituitary gland. 287 23

We have shown in our previous studies that estrogen treatment selectively influences calcitonin gene-related peptide (CGRP)-, methionine-enkephalin (Met-Enk)- and tyrosine hydroxylase (TH)-immunoreactive (IR) intensities in the neurons of the periventricular preoptic nucleus (PPN) and the medial preoptic area (MPA) of the female rat. In the present study, we examined whether estrogen receptor (ER)-IR neurons in the PPN and MPA contain CGRP, Met-Enk, or TH using a double-labeling immunohistochemical method and investigated changes in the number of double-labeling cells upon treatment with estrogen. Brain sections of ovariectomized rats and ovariectomized and estrogen-treated rat were stained using the avidin-biotin-peroxidase complex method followed by the peroxidase-anti-peroxidase method. The sections were first incubated with an anti-ER antibody in conjunction with nickel diaminobenzidine which produces a dark blue reaction product in the nucleus. Subsequently, CGRP, Met-Enk or TH antisera were applied to these sections and the resulting brown diaminobenzidine reaction product in the cytoplasm was examined. Neurons that were double-labeled for ER and CGRP, Met-Enk or TH were investigated in the PPN and MPA. The number of doubly labeled ER/CGRP- and ER/TH-IR neurons was large, whereas the number of ER/Met-Enk-IR neurons was small. These results suggest that ER in the PPN and MPA may be more closely related to the mechanism of changes in CGRP- and TH-IR intensities upon estrogen treatment than that in Met-Enk-IR intensity.
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PMID:Estrogen receptor-immunoreactive neurons contain calcitonin gene-related peptide, methionine-enkephalin or tyrosine hydroxylase in the female rat preoptic area. 772 64

The precise sites and mechanisms by which gonadal steroids influence the activity of neuroendocrine cells controlling pituitary hormone secretion are poorly understood. The present study has determined the distribution of estrogen receptor (ER)-immunoreactive cells in the monkey hypothalamus and examined whether ERs are expressed by luteinising hormone-releasing hormone (LHRH)-and/or dopamine-containing neurones. The distribution of ER-immunoreactive cells was determined in ovariectomised (n = 2) and estrogen plus progesterone-treated (n = 2) cynomolgus macaques and in a single ovariectomised African green monkey. Large numbers of cells immunoreactive for the ER were detected in the preoptic area, bed nucleus of the stria terminalis, periventricular area and ventromedial and arcuate nuclei of all monkeys irrespective of the steroid status. Smaller numbers of ER-immunoreactive cells were found in the paraventricular, but not supraoptic nucleus. Double-labeling experiments in sections from all 5 monkeys revealed that none of the 432 LHRH neurons examined possessed detectable ER immunoreactivity. Neurones stained for tyrosine hydroxylase (TH) were identified in the A11, A12, and A14 cell groups and, although A11 and A12 neurones were intermingled amongst and found adjacent to ER-immunoreactive cells, none of the 1,652 TH-immunoreactive cells examined contained ER immunoreactivity. These results show that ER-immunoreactive cells in the monkey hypothalamus are distributed in a manner similar to that observed in other mammalian species although not all brain regions reported to contain progesterone receptors (PRs) in these species of monkey were found to express ERs. The double-labelling experiments provide further evidence that LHRH neurones do not possess ERs and indicate that, as in other species, estrogen influences on primate LHRH neurones are indirect and/or non-genomic in nature. Unlike the rat and sheep, no evidence was found for ER immunoreactivity in hypothalamic dopaminergic neurones of the monkey. The discrepancy in ER and reported PR receptor localisation within specific hypothalamic nuclei as well as in dopaminergic neurones raises the possibility that not all PR-containing cells may express ERs in the primate hypothalamus.
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PMID:Distribution of estrogen receptor-immunoreactive cells in monkey hypothalamus: relationship to neurones containing luteinizing hormone-releasing hormone and tyrosine hydroxylase. 773 92

In order to assess the neuronal-like properties of a human neuroblastoma cell line obtained by stable transfection of the estrogen receptor (SK-ER3) a series of quantitative measurements of the activity of two neurotransmitter-related enzymes: tyrosine hydroxylase (TH) and monamine oxidase (MAO), and of catecholamine concentrations were performed. When compared to the parental SK-N-BE cell line, the stably transfected SK-ER3 cells show a more pronounced dopaminergic phenotype. The immunoreactivity to a TH antibody is in fact increased and the ratio between dopamine and noradrenaline concentrations is elevated. Treatment with estradiol further enhances the expression of this phenotype. Interestingly, in the transfected cell line MAO-A activity is decreased and further reduced by estrogen treatment. This finding substantiated by previous reports indicates that our model system might represent an interesting tool for the study of the pharmacological treatments of estrogen-induced pathological responses of nervous cells.
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PMID:Estrogen modulation of catecholamine synthesis and monoamine oxidase A activity in the human neuroblastoma cell line SK-ER3. 790 62

In order to elucidate cellular events responsible for sex differentiation of the nigro-striatal system, we studied the influence of estrogen on the expression of tyrosine hydroxylase (TH) in sex-specific dissociated cell cultures of embryonic day 14 rat mesencephalon. Cultures were raised in the absence or presence of 17 beta-estradiol (10(-12) M) and hybridized with a [35S]oligonucleotide specific to TH. Cultured cells and tissues were probed for estrogen receptor (ER) transcripts by hemi-nested PCR. More TH mRNA containing cells were present in control cultures from female than from male donors. Estrogen treatment resulted in an up-regulation of TH expression in male cells only and induced a reversal of the sex difference in TH mRNA levels present in early control cultures. ER message was detectable in hypothalamic and uterine tissues but not in mesencephalic tissue or cultured cells. Estrogen exposure failed to induce ER expression in cultured mesencephalic cells. It is concluded that there are sex differences in TH mRNA expression of developing midbrain dopaminergic neurons which are independent of the steroid environment. Estrogen can up-regulate TH mRNA in a sex-specific fashion by modulating signal transduction mechanisms other than the classical nuclear receptor pathway.
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PMID:Effects of sex and estrogen on tyrosine hydroxylase mRNA in cultured embryonic rat mesencephalon. 877 57

The release of noradrenaline and neuropeptide Y appears to be regulated by estrogen in a co-ordinated fashion within specific brain regions. The present study has used double and triple-labelling immunocytochemical procedures to determine the patterns of nuclear estrogen receptor and neuropeptide Y expression by brainstem A1 and A2 noradrenergic neurons in the female rat. Estrogen receptor-immunoreactive cells were detected within the ventrolateral medulla, nucleus tractus solitarius, area postrema and, in the very caudal medulla, the reticular nuclei and spinal nucleus of the trigeminal nerve. Cells double labelled for the estrogen receptor and dopamine-beta-hydroxylase were identified in largest numbers (up to seven double-labelled cells per 30-microm-thick coronal section) in the caudal-most medulla, where approximately 30% of A1 and 60% of A2 neurons were immunoreactive for the estrogen receptor. These percentages reduced in a linear fashion in more rostral sections and at the level of the area postrema, no co-expression was evident in the ventrolateral medulla and only 10% of A2 neurons displayed estrogen receptor immunoreactivity. Fluorescence double-labelling studies undertaken in colchicine-treated rats revealed that 50% and 90-100% of tyrosine hydroxylase-immunoreactive cells were positive for neuropeptide Y in the rostral ventrolateral medulla and nucleus tractus solitarius (up to 15 double-labelled cells per section), respectively. This pattern of co-expression also showed a rostrocaudal bias, but in the opposite direction, such that none of the caudal-most A1 and only 10% of caudal A2 neurons were immunoreactive for neuropeptide Y. Triple-labelling experiments revealed the presence of a total of only three triple-labelled cells in the ventrolateral medulla and none in the nucleus tractus solitarius of four rats. Double-labelling studies examining estrogen receptor and neuropeptide Y co-expression similarly found only three double-labelled cells in the ventrolateral medulla. These findings provide immunocytochemical evidence for a clear rostrocaudal topography in nuclear estrogen receptor synthesis by A1 and A2 neurons and show a reverse rostrocaudal bias in neuropeptide Y expression by these cells. The absence of any substantial neuropeptide Y and estrogen receptor co-expression in A1 and A2 neurons indicates that these two proteins are very likely to be differentially expressed by brainstem noradrenergic neurons. Such observations provide further evidence for the biosynthetic and functional heterogeneity of brainstem noradrenergic cells and suggest that A1 and A2 neurons transmitting information on estrogen status within the brain are unlikely to utilize neuropeptide Y as a co-transmitter.
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PMID:Differential expression of estrogen receptor and neuropeptide Y by brainstem A1 and A2 noradrenaline neurons. 901 35

A double immunocytochemical procedure, with two different chromogens, was used to compare the respective distribution of estrogen receptor-immunoreactive cells and tyrosine hydroxylase-immunoreactive neurons on the same sections of the preoptic region of adult female rainbow trout (Oncorhynchus mykiss). Estrogen receptor-immunoreactive cells were observed in the anterior preoptic region surrounding the preoptic recess and its large lateral extensions. Tyrosine hydroxylase-immunoreactive cells were consistently detected in the ventral and ventrolateral walls of the preoptic recess, in an area that was named nucleus preopticus pars anteroventralis. Dopamine immunohistochemistry and Dil retrograde transport studies indicated that part of these catecholaminergic neurons are dopaminergic and could project to the pituitary. Double staining studies showed consistently that most estrogen receptor-positive cells located ventral to the large extensions of the preoptic recess are also tyrosine hydroxylase-positive, indicating that this region is a major target for estradiol feedback. The results are discussed in relation to the role of the nucleus preopticus pars anteroventralis in mediating the negative feedback actions of estradiol on the secretion of gonadotrophin (GTH2) secretion. A hypothesis is drawn in order to explain the synchronizing role of estradiol at the time of ovulation in rainbow trout.
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PMID:Estrogen receptors are expressed in a subset of tyrosine hydroxylase-positive neurons of the anterior preoptic region in the rainbow trout. 905 80

The neural components underlying the influence of photoperiod upon reproductive functioning are poorly understood. In this study, we have used immunocytochemistry to examine whether changes in photoperiod may influence specific neuronal cell populations implicated in mediating gonadal steroid feedback actions on GnRH neurons. Short day (SD) exposed ewes in the midluteal stage of the estrous cycle and long day (LD) anestrous ewes were perfused in pairs and hypothalamic brain sections immunostained for tyrosine hydroxylase (TH), neuropeptide Y (NPY), beta-endorphin (betaE), and the estrogen receptor (ER). The number of ER-immunoreactive cells detected within the preoptic area, but not the hypothalamus, was approximately 20% higher (P < 0.05) in LD ewes compared with SD animals. The numbers of TH-immunoreactive neurons comprising the A12, A14, and A15 cell groups were not different between LD and SD ewes, and the percentage of A12 (approximately 15%) and A14 (approximately 25%) neurons expressing ERs was similarly unaffected by photoperiod. The number of betaE neurons detected in the arcuate nucleus was 50% lower (P < 0.05) in SD vs. LD ewes, whereas NPY-immunoreactive cell numbers in the median eminence were 300% higher (P < 0.05). Approximately 3% of NPY neurons in the median eminence, and 10% in the arcuate nucleus, expressed ER immunoreactivity in a photoperiod-independent manner. These studies indicate that changes in photoperiod may regulate ER expression within the preoptic area and suggest that hypothalamic NPY and betaE neurons are involved in the seasonal regulation of reproductive activity in the ewe.
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PMID:Effects of photoperiod on estrogen receptor, tyrosine hydroxylase, neuropeptide Y, and beta-endorphin immunoreactivity in the ewe hypothalamus. 916 52


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