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)

The anlages of the medial-basal hypothalamus (MBH), septopreoptic area (POA), Rathke's pouch, and the parietal cortex (CC) of rats (at 12.5, 14.5 and 16.5 days of gestation) were transplanted singly or in combination into the third ventricle of adult female rats, and the development of neurons in the grafts was investigated immunohistochemically with the use of antisera to tyrosine hydroxylase (TH), somatostatin (SRIH), ACTH, methionine enkephalin-Arg6-Gly7-Leu8 (Enk-8), rat corticotropin-releasing factor (rCRF), rat hypothalamic growth hormone-releasing factor (rhGRF), and luteinizing hormone-releasing hormone (LHRH). TH and all the peptides examined except LHRH were detected in distinct neurons in MBH grafts and in cografts of MBH plus Rathke's pouch from 12.5-day-old embryos. SRIH, rCRF, Enk-8, and TH were found in POA grafts from embryos of the same age. Although immunoreactive LHRH was first detected in neurons in POA grafts from 16.5-day-old embryos, it appeared in cografts of POA and MBH from 12.5-day-old embryos. The immunoreactive fibers developed in the grafts expressed the same characteristic behaviors as in intact brain; the fibers containing hormonal substances formed complexes with the vasculature like in the organum vasculosum laminae terminalis (OVLT) or in the median eminence, while the fibers containing neurotropic signals formed fiber networks surrounding other nerve cell bodies as if they synaptically associate. In CC grafts, the neurons contained TH, SRIH, rCRF, or Enk-8, and their axonal processes formed fiber networks. These findings suggest that all the hypothalamic neurons examined are committed by 12.5 days of gestation to develop maintaining transmitter phenotype and target recognition capacity.
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PMID:Development of hypothalamic neurons in intraventricular grafts: expression of specific transmitter phenotypes. 289 28

Corticotropin-releasing factor (CRF) caused a concentration-dependent increase in dopamine (DA) synthesis measured in rat striatal synaptosomes. The concentrations of CRF producing half-maximal and maximal stimulation were 40 and 300 nM, respectively. The maximal effect corresponded to a 34% increase from the control level of DA synthesis. CRF 1 microM increased DA synthesis in synaptosomes of mouse striatum by 48%. Pretreatment of striatal synaptosomes with CRF produced a persistent activation of tyrosine hydroxylase assayed in extracts of lysed synaptosomes. These results suggest that CRF may play a modulatory role in striatal DA synthesis by acting on receptors located on DA terminals.
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PMID:Corticotropin-releasing factor activates tyrosine hydroxylase in rat and mouse striatal homogenates. 290 59

The distribution of neurons and fibres that contain substance P, cholecystokinin-8, vasoactive intestinal polypeptide, corticotropin-releasing factor, calcitonin-gene-related peptide, choline acetyltransferase, tyrosine hydroxylase, somatostatin, leucine-enkephalin, and neuropeptide Y was examined in the parabigeminal nucleus of the rat by immunohistochemistry. Many choline acetyltransferase-like immunoreactive or calcitonin-gene-related peptide-like immunoreactive neurons were observed in the dorsal, middle and ventral subdivisions of the parabigeminal nucleus. A few corticotropin-releasing factor-like immunoreactive neurons were also seen in these three subdivisions. The double-immunostaining demonstrated that some choline acetyltransferase-like immunoreactive neurons in the dorsal and ventral subdivisions contained calcitonin-gene-related peptide. Fibres containing cholecystokinin-8, substance P or vasoactive intestinal polypeptide were abundant in the parabigeminal nucleus. Fibres containing cholecystokinin-8 were concentrated in the dorsal and ventral subdivisions, and the lateral margin of the middle subdivision, whereas many fibres containing substance P or vasoactive intestinal polypeptide existed in the lateral half of each subdivision. Fibres containing calcitonin-gene-related peptide or corticotropin-releasing factor were mostly observed around the immunoreactive neurons. Tyrosine hydroxylase-like immunoreactive fibres were scattered in the parabigeminal nucleus.
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PMID:Localization of neuroactive substances in the rat parabigeminal nucleus: an immunohistochemical study. 290 92

Steroid hormones modify several brain functions, at least in part by altering expression of particular genes. Of interest are those genes that are involved in cell-cell communication in the brain, for instance neuropeptide genes and genes that code for enzymes involved in synthesis of neurotransmitters. Steroid regulation of mRNA levels for several genes has been reported, including the genes coding for the neuropeptides vasopressin, corticotropin releasing factor, luteinizing hormone-releasing factor, pro-opiomelanocortin; somatostatin, preproenkephalin, and the enzyme tyrosine hydroxylase. Steroid control of releasing factor genes is consistent with classical neuroendocrine concepts of negative feedback. Steroid-induced plasticity of gene expression is sometimes in evidence, with the presence or absence of a particular steroid inducing expression of a neuropeptide gene in neurons that under other conditions do not express the gene. As a means of gaining some insight into the mechanism of action of steroid hormones, several groups have determined some of the neuropeptide profiles of neurons that contain receptors for steroid hormones. Marked heterogeneity is found, in that often only a subpopulation of phenotypically-similar neurons, even within a single brain area, contains receptors for a given steroid.
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PMID:Regulation of neuropeptide gene expression by steroid hormones. 307 66

The changes in dopamine catabolites in various regions of mouse brain have been studied following a variety of behavioral treatments. In confirmation of the results of many others, we find that treatments such as footshock or restraint result in a pronounced activation of dopaminergic systems in the prefrontal cortex, as determined by increases in the content of DOPAC (3,4-dihydroxyphenylacetic acid). However, we also find small but statistically significant increases of DOPAC in the hypothalamus and brain stem even with mild treatments. With restraint and more intense footshock we observe increases of DOPAC in all regions studied, including nucleus accumbens, olfactory tubercle, amygdala, and the striatum. Thus in contrast to previous reports, we find that the DA response in stress is global like that of norepinephrine [as determined by increases of 3-methoxy,4-hydroxyphenylethyleneglycol, (MHPG)], and not specific to the prefrontal cortex. The activation of prefrontal cortex DA metabolism is associated with an activation of the synthetic enzyme tyrosine hydroxylase. The response pattern of catecholamine metabolites is similar following a variety of stressors, including conditioned footshock, training with one footshock in passive avoidance behavior, performance of passive avoidance behavior, and even following exposure to an apparatus in which mice have been shocked previously. Injection of mice with Newcastle disease virus increases plasma corticosterone, and DOPAC and MHPG in the hypothalamus and brain stem, but not the prefrontal cortex. Thus a virus infection can be considered a stressor. Furthermore, intracerebroventricular (ICV) injection of corticotropin-releasing factor (CRF) produces stresslike increases in DOPAC and MHPG concentrations, suggesting that the release of CRF in the brain during stress may mediate the changes in catecholamine metabolism.
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PMID:Stress-related activation of cerebral dopaminergic systems. 320 43

In vitro studies of rat brain tyrosine hydroxylase and tryptophan hydroxylase activities have demonstrated nonlinearities in both time course and substrate velocity curves that were sensitive to small changes in tetrahydrobiopterin (BH4) concentrations when studied within a range speculated to approximate the in vivo condition. High-performance liquid chromatographic determinations of rat striatal BH4 levels reported here are consistent with such a nonlinear relationship of BH4 and brain monoamine synthesis under four in vivo conditions: 1-day s.c. amphetamine infusion, L-tryptophan loads, i.v.t. administration of corticotropin releasing factor and the diurnal rhythms of the dopaminergic nigrostriatal and serotonergic raphe hippocampal systems. Only the results of continuous 10-day amphetamine infusion were consistent with a simple stoichiometric relationship between the (postulated) rate limiting concentrations of BH4 and regional levels of brain monoamines. Although some of the statistically significant changes in regional brain BH4 levels are small, previous reports of the failure of biopterin to change in response to more than 30 other central nervous system drugs, including such stimulants as methylphenidate and cocaine, makes them noteworthy.
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PMID:Relationships between drug-induced changes in tetrahydrobiopterin and biogenic amine concentrations in rat brain. 387 80

A decrease of corticotropin-releasing factor (CRF) concentration has been reported in patients with Parkinson's disease (PD). The present study further examined the role of CRF in an animal model of parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Results indicated that both subchronic (2 days) and chronic (7 days) MPTP treatments decreased the number of CRF immunoreactive neurons in both the paraventricular nucleus (PVN) of the hypothalamus and the central nuelcus of the amygdala (ACN). This effect lasted for almost a month after withdrawal of chronic MPTP injections. In addition, nomifensine pretreatment protected against MPTP's toxicity on DA neurons, as assessed by tyrosine hydroxylase immunoreactivity in the substantia nigra. However, the same treatment did not prevent the toxicity of MPTP on CRF neurons. Further, no significant difference was notable in the number of CRF immunoreactive neurons between normal young adult and normal middle-aged rats in both the PVN and the ACN. These results suggest that MPTP also produces a neurotoxicity on CRF neurons, and this effect is not secondary to MPTP's effect on DA neurons. Besides, altered CRF neuronal activity is involved in the process of pathological ageing, but not physiological ageing. Further, reduced CRF immunoreactivity in the PVN and ACN may imply alterations of neuroendocrine, autonomic as well as central functions caused by MPTP.
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PMID:Alteration of corticotropin-releasing factor immunoreactivity in MPTP-treated rats. 747 78

Morphine dependence was experimentally induced in rats by daily injection of increasing doses of morphine for seven days. Withdrawal was precipitated in half of the morphine-dependent rats by a single injection of naloxone on day 8. Behavioral signs of withdrawal were evident in the morphine/naloxone group. Gene expression in locus coeruleus (LC) neurons was investigated using quantitative in situ hybridization analysis. Messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis, and for precursors to galanin (GAL) and neuropeptide Y (NPY), peptides that coexist with norepinephrine in LC neurons, were not altered by chronic morphine treatment or naloxone-precipitated withdrawal. In contrast, mRNA levels for c-fos were dramatically elevated in the LC following naloxone-precipitated withdrawal. Chronic morphine treatment caused a small decrease in levels of mRNA encoding the precursor to corticotropin-releasing factor (CRF) in Barrington's nucleus. Although long-term adaptations of LC neurons have previously been implicated in the development of morphine tolerance, dependence, and withdrawal, alterations in the levels of TH, GAL, or NPY mRNA in the LC apparently do not underlie this process.
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PMID:Lack of effect of chronic morphine treatment and naloxone-precipitated withdrawal on tyrosine hydroxylase, galanin, and neuropeptide Y mRNA levels in the rat locus coeruleus. 754 Mar 19

The hypothalamus has been claimed to be involved in a great number of physiological functions in development, such as sexual differentiation (gender, sexual orientation) and birth, as well as in various developmental disorders including mental retardation, sudden infant death syndrome (SIDS), Kallman's syndrome and Prader-Willi syndrome. In this review a number of hypothalamic nuclei have therefore been discussed with respect to their development in health and disease. The suprachiasmatic nucleus (SCN) is the clock of the brain and shows circadian and seasonal fluctuations in vasopressin-expressing cell numbers. The SCN also seems to be involved in reproduction, adding interest to the sex differences in shape of the vasopressin-containing SCN subnucleus and in its VIP cell number. In addition, differences in relation to sexual orientation can be seen in this perspective. The vasopressin and VIP neurons of the SCN develop mainly postnatally, but as premature children may have circadian temperature rhythms, a different SCN cell type is probably more mature at birth. The sexually dimorphic nucleus (SDN, intermediate nucleus, INAH-1) is twice as large in young male adults as in young females. At the moment of birth only 20% of the SDN cell number is present. From birth until two to four years of age cell numbers increase equally rapidly in both sexes. After this age cell numbers start to decrease in girls, creating the sex difference. The size of the SDN does not show any relationship to sexual orientation in men. The large neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. In the fetus these hormones play an active role in the birth process. Fetal oxytocin may initiate or accelerate the course of labor. Fetal vasopressin plays a role in the adaptation to stress--caused by the birth process--by redistribution of the fetal blood flow. Corticotropin-releasing hormone (CRH) neurons of the PVN play a central role in stress response. Thus fetal CRH neurons may play a role in the timing of the moment of birth. Recently, alterations have been described in peptidergic, aminergic and cholinergic transmitters in the hypothalamus in SIDS. Future research will have to establish whether these changes are part of the course of SIDS. A large proportion of the SON and PVN neurons also produce tyrosine hydroxylase (TH). In neonates the majority of TH-immunoreactive neurons colocalizes vasopressin, while in the adult the majority of TH-positive neurons colocalizes oxytocin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Development of the human hypothalamus. 764 57

The participation of sympathetic adrenal innervation in the control of the neonatal adrenocortical system and in changes in adrenal sensitivity after maternal separation for 24 h was tested in 10- and 23-day-old pups. Chemical sympathectomy by guanethidine (20 mg/kg body wt) decreased basal and stimulated corticosterone compound B (B) secretion without affecting adrenocorticotropic hormone (ACTH) release, abolished the enhanced adrenal sensitivity to ACTH induced by maternal separation in 10-day-old pups, but did not modify adrenal sensitivity following ether stress in 23-day-old pups. Guanethidine treatment did not affect body and adrenal weight or adrenal choline acetyltransferase activity, but it increased tyrosine hydroxylase activity at both ages. Both chronic guanethidine treatment and acute corticotropin-releasing factor immunoneutralization reduced plasma B levels after maternal separation without affecting plasma ACTH levels. Maternal separation in 10-day-old pups enhanced basal and stimulated ACTH and B secretion after exposure to ether vapors and insulin-induced hypoglycemia (IIH). In nonseparated pups, IIH did not stimulate ACTH secretion and caused small increases in B secretion; however, the enhanced response of separated pups to IIH was due to the effects of intraperitoneal injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chemical sympathectomy and maternal separation affect neonatal stress responses and adrenal sensitivity to ACTH. 777 91


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