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)

Control of growth hormone (GH) and prolactin (PRL) release was investigated in hypophysial stalk-transected (HST) and stalk-intact pigs by determining the effects of analogs of GH-releasing factors (GHRF), somatostatin (SRIF), arginine, thyrotropin-releasing hormone, alpha-methyl-rho-tyrosine, and haloperidol. HST and control gilts were challenged with intravenous injections of human pancreatic GHRF(1-40)OH, thyrotropin-releasing hormone, and analogs of rat hypothalamic GHRF. HST animals remained acutely responsive to GHRF by releasing 2-fold greater quantities of GH than seen in controls. This occurred in spite of a 38% reduction in pituitary gland weight and a 32 and 55% decrease in GH concentration and total content. During SRIF infusion, GH remained at similar basal concentrations in HST and control gilts, but increased immediately after stopping SRIF infusion only in the controls. Releasable pituitary GH appears to accumulate during SRIF infusion. GHRF given during SRIF infusion caused a 2-fold greater release of GH than seen in animals receiving only GHRF. Arginine increased (P less than 0.05) GH release in controls, but not in HST gilts, which suggests that it acts through the central nervous system. Basal PRL concentrations were greater (P less than 0.05) in HST gilts than in control gilts. TRH acutely elevated circulating PRL (P less than 0.001) in HST gilts, suggesting that it acts directly on the pituitary gland. Haloperidol, a dopamine receptor antagonist, increased circulating PRL in controls but not in HST animals. alpha-Methyl-rho-tyrosine did not consistently increase circulating PRL, however, suggesting that it did not sufficiently alter turnover rate of the tyrosine hydroxylase pool. The results indicate that the isolated pituitary after HST remains acutely responsive to hypothalamic releasing and inhibiting factors for both GH and PRL release in the pig.
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PMID:Growth hormone and prolactin secretion in hypophysial stalk-transected pigs as affected by growth hormone and prolactin-releasing and inhibiting factors. 167 Dec 98

Spontaneous dwarf mice, in which both growth hormone (GH) and prolactin (PRL) are undetectable, are severely deficient in the PRL-inhibiting catecholamine dopamine (DA), as well as its synthetic enzyme, tyrosine hydroxylase (TH), in the basal hypothalamus (Phelps et al., Cell Tissue Res., 240:19-25, 1985; Phelps, Brain Res., 416:354-358, 1987). In contrast, transgenically constructed dwarf mice (Behringer et al., Genes Dev., 2:453-461, 1988) show complete ablation of pituitary GH cells, but PRL cells are retained at a level of approximately 10% of normal. In order to determine the feedback effect of this reduced, rather than absent, PRL on hypothalamic DA neurons, brains of transgenic dwarf mice were examined for catecholamine transmitters by histofluorescence, for the synthetic enzyme TH by immunocytochemistry, and for TH mRNA expression by in situ hybridization. DA histofluorescence in transgenic dwarfs was comparable to that of normal littermate mice in nonpituitary regulating areas (perikarya of zona incerta [A13] of hypothalamus and in midbrain substantia nigra area [A9]). Arcuate nucleus (A12) DA neurons that inhibit PRL secretion, however, showed dim to absent fluorescence in perikarya and in external median eminence terminals in dwarfs. There were reduced (P less than 0.05) numbers of A12 TH-immunoreactive neurons in transgenic dwarfs, to approximately 60% of those in normal mice. In contrast, TH-positive neurons in other hypothalamic areas (A13, A14) had average populations equivalent to those in normal mice. Quantification of TH mRNA abundance by in situ hybridization using both image analysis of hybridization over the arcuate nucleus, and grain counts per individual A12 cell in this nucleus, indicated that relative mRNA levels were the same in normal and transgenic dwarfs. The observations indicate that reduction in pituitary PRL is accompanied by defective expression in hypothalamic tuberoinfundibular neurons, which is severe at the DA neurotransmitter level, significant regarding observable TH immunoreactivity, and undetectable with regard to TH mRNA expression. Collectively, the findings suggest that posttranscriptional processes are involved with the mediation of PRL feedback upon hypothalamic neurons. Technically and quantitatively, the report presents the feasibility of simultaneous evaluation of transmitter histofluorescence, synthetic enzyme immunocytochemistry, and mRNA expression in individual animals.
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PMID:Hypothalamic dopaminergic neurons in transgenic dwarf mice: histofluorescence, immunocytochemical, and in situ hybridization studies. 168 35

We have shown that the endogenous neuropeptides, growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) influence expression of both cholinergic and catecholaminergic neuronal phenotypes in developing chick brain as assessed by the activities of choline acetyltransferase and tyrosine hydroxylase, respectively (Dev. Brain Res., 49 (1989) 275-280; Brain Research, 512 (1990) 297-303). In this study we examined the effects of GHRH and SRIF on GABAergic neuronal expression in ovo using activity of glutamate decarboxylase (GAD) as a neuronal marker. Chick embryos were administered GHRH or SRIF in ovo via the air sac on embryonic days 1, 3, 5 and 7, sacrificed at day 8 and the activity of GAD assayed in whole brain homogenates. GAD activity was significantly reduced in peptide-treated embryos as compared to controls. Similar results were obtained when GHRH was administered in a single dose at days 1 or 3 or when SRIF was administered in a single dose at day 3; GAD activity was significantly reduced as compared with control embryos. In contrast, embryos treated with either GHRH or SRIF on day 5 of development showed no difference in GAD activity as compared to controls. These data support our previous findings that endogenous neuropeptides such as GHRH and SRIF possess important properties with respect to neuronal phenotypic expression. They further define the critical period of sensitivity to these neuropeptides as 1-3 days of embryonic development.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone-releasing hormone and somatostatin influence neuronal expression in developing chick brain. III. GABAergic neurons. 168 48

In a previous study we have shown that in ovo administration of growth hormone-releasing hormone (GHRH) influences catecholaminergic neuronal expression as assessed by tyrosine hydroxylase activity (Dev. Brain Res., 49 (1989) 275-280). In this study we examined the effects of GHRH and somatostatin (SRIF) on cholinergic neuronal neurotransmitter expression both in ovo and in vitro. Chick embryos were administered GHRH or SRIF in ovo via the air sac on embryonic days 1, 3, 5 and 7, sacrificed at day 8 and the activity of choline acetyltransferase (ChAT) was assayed in whole brain homogenates. ChAT activity was significantly higher in peptide-treated embryos as compared to controls. Similar results were obtained when GHRH or SRIF (50 ng/50 microliters) was administered in a single dose at day 2 or 3; ChAT activity was significantly increased in peptide-treated versus control embryos. In contrast, embryos treated with GHRH or SRIF on day 1 or 5 or with growth hormone (100 ng/50 microliters) on day 3 of incubation showed no difference in ChAT activity as compared to controls. More direct effects of GHRH and SRIF were tested in neuron-enriched cultures derived from 3- (E3) or 6-day-old (E6) chick embryos. Cultures were grown in either serum-supplemented or serum-free medium for 6 days in the presence of GHRH or SRIF concentrations ranging from 0.01 to 100 nM. As observed in ovo, ChAT activity was increased in E3 cultures treated with peptides. In addition, the composition of the culture medium influenced the response to peptide treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone-releasing hormone and somatostatin influence neuronal expression in developing chick brain. II. Cholinergic neurons. 197 43

Ames dwarf mice do not synthesize or release growth hormone or prolactin (PRL) and have very poorly developed tuberoinfundibular dopaminergic (TIDA) neurons. An antibody to tyrosine hydroxylase (TH), the rate-limiting enzyme in the biosynthesis of dopamine, and immunohistochemical procedures were used in this study to compare the numbers of TH-immuno-positive neurons observed in the arcuate nuclei of Ames dwarf mice compared to phenotypically normal mice of the same strain. In female dwarfs, the number of TH-immunopositive neurons in the arcuate nuclei but not the pars compacta was markedly reduced when compared to normal females. The elevation of circulating PRL either by the implantation of a normal pituitary under the kidney capsule or by the daily administration of ovine PRL increased the numbers of arcuate neurons which expressed immunochemically detectable TH to a level comparable to that observed in untreated normal mice. The number of TH-expressing neurons was also reduced in the arcuate nuclei of dwarf males although the deficiency was not as great as in females. Ovine PRL seemed to have little effect on the numbers of TH-immunopositive neurons observed in either dwarf or normal male mice. These results suggest that the postnatal absence of PRL in mice does not result in a major reduction in the total population of TIDA neurons. Rather these neurons appear to be present in nearly normal numbers but are in a dormant state in the absence of circulating PRL.
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PMID:Effect of prolactin replacement on the number of tyrosine hydroxylase expressing neurons in the arcuate nuclei of Ames dwarf and normal mice. 197 56

We have examined the influence of ethanol on cholinergic and catecholaminergic neuronal expression in the chick embryonic brain using choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) activities as respective neuronal markers. Ethanol (5-20 mg/50 microliters/day), administered to embryos in ovo from day 1 to 3 of development produced a dose-dependent decrease in ChAT activity while TH activity exhibited a dose-dependent increase when embryos were sacrificed on embryonic day 8. The optimal neurotoxic dose of ethanol following this paradigm was 15 mg/day and the LD50 was 17.5 mg/day for the 3 days. Subsequently, embryos were administered ethanol (15 mg) either alone or concomitantly with growth hormone-releasing hormone (GH-RH; 100 ng/50 microliters/day). Previous studies from this laboratory have demonstrated both potent cholinotropic and catecholaminotropic effects for this neuropeptide, results confirmed in this study. Co-administration of ethanol and GH-RH resulted in a significant increase in ChAT activity as compared to both saline- and ethanol-treated controls when examined on day 8 of embryonic growth. No additive effect was observed in TH activity following co-administration of ethanol and GH-RH. The findings from this study are interpreted to mean that GH-RH represents a potent secondary signal to undifferentiated neuroblasts which may lead to a restoration of the cholinergic neuronal population following neurotoxic insult by ethanol.
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PMID:Neuronal plasticity in the developing chick brain: interaction of ethanol and neuropeptides. 197 60

We have examined catecholaminergic expression during development in the chick embryonic brain using tyrosine hydroxylase (TH) activity as a biochemical marker for catecholaminergic neurons. TH activity was detectable as early as after 4 days of incubation in whole brain homogenates and increased throughout embryonic development. The greatest increase in enzyme activity was observed between embryonic days 8 and 15, a period of active neuronal maturation and synaptogenesis. Growth hormone-releasing hormone (GHRH) was tested for its influence on TH activity during embryonic development. Eight-day-old embryos that received GHRH (50 ng/50 microliters) in ovo on days 1, 3, 5 and 7 exhibited a significant (P less than 0.001) increase in TH activity. Similar results were obtained when GHRH was administered in a single 50 ng/50 microliter dose on day 1 or day 3 of development. However, embryos receiving the same dose of GHRH on day 5 exhibited no significant difference in TH activity as compared to controls. When growth hormone (GH, 100 ng/50 microliters) was administered during the same critical period (day 3) no difference was observed in TH activity as compared to controls. Thus, the effects of GHRH on TH activity do not appear to be mediated through GH. We interpret these data to mean that GHRH can enhance catecholaminergic phenotypic expression in the chick embryonic brain when administered during a discrete critical period of development from days 1 to 3 of embryonic age.
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PMID:Growth hormone-releasing hormone influences neuronal expression in the developing chick brain. I. Catecholaminergic neurons. 257 59

Immunocytochemistry revealed growth hormone-releasing hormone (GRF)-containing cells (4-10/50 microns thick coronal sections) in the ventral portion of the medial parvicellular subdivision of the paraventricular nucleus (PVN) in the rat. In the same region we also detected about the same number of neurons containing the mRNA that encodes GRF using in situ hybridization histochemistry. Fluorescence double labelling immunohistochemistry showed the presence of GRF and tyrosine hydroxylase (TH) in the same PVN neurons. The overlap between the two populations of cells is only partial: less than half of TH-positive cells contain GRF and vice versa.
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PMID:Partial coexistence of growth hormone-releasing hormone and tyrosine hydroxylase in paraventricular neurons in rats. 257 94

The distribution of growth hormone-releasing factor (GRF) and tyrosine hydroxylase (TH), a marker for dopamine neurons in this region, was analyzed in the mediobasal hypothalamus with indirect immunofluorescence histochemistry and an elution-restaining procedure. TH-like immunoreactivity was present in most GRF-immunoreactive cells in the ventral part of the arcuate nucleus (ventral A12 dopamine cell group). Dopamine cells in the dorsal A12 group and, for example, in the hypothalamic A14 cell group seemed to lack GRF peptide. Partly overlapping GRF- and TH-immunoreactive fibers in the median eminence were observed, indicating possible coexistence of the two compounds also in nerve endings close to portal vessels. These findings suggest that a subpopulation of A12 dopamine neurons produces, stores and releases a GRF-like peptide. Possible interactions of GRF and dopamine in the control of growth hormone secretion are discussed.
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PMID:Coexistence of tyrosine hydroxylase and growth hormone-releasing factor in a subpopulation of tubero-infundibular neurons of the rat. 286 25

Rett syndrome is an increasingly recognized progressive disorder in females, commencing in infancy and characterized by autistic behavior, gait ataxia, stereotyped movements, seizures and generalized growth and mental retardation, possibly associated with disorders of central biogenic amine synthesis. The gene locus and pathogenesis of Rett syndrome are unknown. Autopsy studies in nine girls dying between 4 and 17 years, and sural nerve and muscle biopsies from two girls aged 3 and 17 years showed: (1) diffuse cortical atrophy/micrencephaly, with a decrease in brain weight by 12% to 34% of age-matched controls, apparently related to the duration of the disorder; (2) mild diffuse cortical atrophy with increased amounts of neuronal lipofuscin and occasional mild gliosis, but without signs of a storage disorder; (3) underpigmentation of the zona compacta nigrae, which showed fewer well-pigmented neurons for age and fewer melanin granules per neuron, while total numbers of nigral neurons and the substructure of neuromelanin were normal for age. No pathological changes were seen in other transmitter-specific brain stem nuclei; (4) immunoreactivity for tyrosine hydroxylase was slightly reduced in nigral and hypothalamic neurons, and the pituitary gland showed decreased immunoreaction for prolactin and growth hormone; (5) ultrastructurally, in frontal cortex and caudate nucleus, isolated abnormal neurites and reactive or degenerative axonal swellings were seen; the latter are possibly related to the nigral changes, suggesting some dysfunction of the dopaminergic nigrostriatal system, which is supported by neurochemical data; (6) preliminary biochemical studies revealed increased beta-endorphines in thalamus and cerebellum; (7) peripheral nerves demonstrated increase in small fibers without demyelination and increased numbers of neurofilaments in axons, suggesting distal axonopathy, while skeletal muscle showed alterations in the sarcoplasmic reticulum with circular profiles in the Z-filaments. These nonspecific changes may be interpreted as early signs of denervation. The variety of lesions in the central, neuroendocrine and peripheral neuromuscular systems in Rett syndrome are discussed with regard to their clinical and biochemical significance.
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PMID:Neuropathology of Rett syndrome. 290 May 87


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