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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously reported that the human melanoma cell line, SEKI, induces severe weight loss in nude mice. In the present study, we examined the expression of weight-regulating neuropeptide mRNAs in the hypothalamus of this cancer cachectic model by using a sensitive quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method and in situ hybridization. mRNA levels of neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) in the whole hypothalamus were elevated significantly in the SEKI mice as compared with control mice. In situ hybridization showed that NPY and CRH mRNA were upregulated in the arcuate nucleus and the paraventricular nucleus, respectively. There were no significant differences in melanin-concentrating hormone (MCH), orexin (OX), and cholecystokinin mRNA levels between the SEKI and control mice. These results suggest that the NPYergic system is functioning in the rodent model of cancer cachexia; however, the role of the CRHergic system in energy homeostasis remains to be elucidated. This is the first report of the hypothalamic neuropeptide response to cachexia-inducing human cells.
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PMID:Hypothalamic appetite-regulating neuropeptide mRNA levels in cachectic nude mice bearing human tumor cells. 1158 96

Cortical spreading depression (CSD) may be the underlying mechanism of migraine aura. The role of CSD in initiating a migraine headache remains to be determined, but it might involve specific changes in gene expression in the brain. To examine these changes, four episodes of CSD at 5-minute intervals were induced in the mouse brain by application of 300mM KCl, and gene expression was examined 2 hours later using cDNA array and reverse transcriptase-polymerase chain reaction. Controls consisted of groups that received anesthesia only, attachment of recording electrodes only, and application of 0.9% NaCl. Of the over 1,180 genes examined in our experiments, those consistently regulated by CSD included vasoactive peptides; the vasodilator atrial natriuretic peptide was induced by CSD, while the vasoconstrictor neuropeptide Y was downregulated. Other genes specifically regulated by CSD were involved in oxidative stress responses (major prion protein, glutathione-S-transferase-5, and apolipoprotein E). L-type calcium channel mRNA was upregulated. In summary, CSD regulates genes that are intrinsic to its propagation, that identify accompanying vascular responses as a potential source of pain, and that protect against its potential pathological consequences. We believe these observations have strong relevance to the mechanisms of migraine and its outcomes.
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PMID:Cortical spreading depression and gene regulation: relevance to migraine. 1192 Oct 56

Pituitary pars intermedia melanotrope cells are often used as a model to study mechanisms of neuroendocrine integration. In the amphibian Xenopus laevis, the synthesis and release of alpha-melanophore-stimulating hormone (alpha-MSH) from these cells is a dynamic process dependent upon the colour of background. In animals on a black background, there is a higher level of synthesis and secretion of alpha-MSH than in animals on a white background, and, consequently, there is skin darkening in animals on a black background. The melanotropes are innervated by hypothalamic neurones that produce neuropeptide Y (NPY), a peptide that inhibits alpha-MSH secretion via the NPY Y1 receptor. The inhibitory neurones have a higher expression of NPY in animals adapted to a white background and both the size and the number of inhibitory synapses on the melanotrope cells are enhanced. The purpose of the present study was to determine if this presynaptic plasticity displayed by the inhibitory neurones is reciprocated by postsynaptic plasticity (i.e. if there is an enhanced expression of the Y1 receptor in melanotropes of animals adapted to a white background). For this purpose quantitative real-time reverse transcriptase-polymerase chain reaction was used to determine the level of Y1 receptor mRNA in melanotropes of animals undergoing the process of background adaptation. The results showed that there is a higher Y1 receptor mRNA expression in melanotropes of white-adapted animals. We conclude that the inhibitory neuroendocrine interface in the Xenopus pars intermedia displays postsynaptic plasticity in response to changes of background colour. To our knowledge, this is the first demonstration of a physiological environmental change leading to changes in postsynaptic receptor expression in a fully identified vertebrate neuroendocrine reflex.
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PMID:Demonstration of postsynaptic receptor plasticity in an amphibian neuroendocrine interface. 1242 36

Immunoreactivities (IR) for catecholamine-synthesizing enzymes tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DbetaH), phenylethanolamine N-methyl transferase (PNMT), serotonin-synthesizing enzyme tryptophan hydroxylase, and neuropeptide Y were investigated in the intrinsic cardiac nervous system of 27-40-day-old rats using fluorescent immunohistochemistry. Individual neurons were identified by the general neuronal marker protein gene product 9.5. The presence of DbetaH and PNMT in the atrial specimens was verified using reverse transcriptase-polymerase chain reaction. Two types of catecholamine-handling intrinsic ganglion neurons were observed: small intensely fluorescent (SIF) cells and large-diameter neurons. SIF cells exhibited TH- and tryptophan hydroxylase-IR, but they were not positive for DbetaH. In contrast, large-diameter intrinsic TH-positive neurons, showing in majority also NPY-IR, displayed also DbetaH- and PNMT-IR, thus indicating the capacity for the synthesis of norepinephrine and epinephrine, respectively. In conclusion, the SIF cells are most probably dopaminergic and serotonergic neurons, whereas large-diameter intrinsic cells seem to represent a subpopulation of norepinephrine- and/or epinephrine-secreting neurons.
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PMID:Catecholaminergic neurons in the rat intrinsic cardiac nervous system. 1267 49

Exogenous neuropeptide Y produced marked contractions in rat isolated common jugular, brachial, and caudal veins, while it produced little or no contractions in common carotid, brachial, and caudal arteries. Neuropeptide Y (30 nM) produced larger contractions in these veins than did phenylephrine (1 microM), with maximal contractions through the neuropeptide Y receptor and the alpha1-adrenoceptor, respectively. In contrast, neuropeptide Y (30 nM) produced smaller contractions than did phenylephrine (1 microM) in the arteries. Pre-treatment with neuropeptide Y (30 nM) showed remarkable desensitization to neuropeptide Y (30 nM). This desensitization lasted for 1 h in the caudal vein or for 2 h in the common carotid and brachial veins. The neuropeptide Y-induced contraction and its desensitization probably occurred through the neuropeptide Y receptor subtype Y1, because only the neuropeptide Y receptor subtype Y1 was detected in the smooth muscle by the reverse transcriptase-polymerase chain reaction.
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PMID:Neuropeptide Y-induced contraction and its desensitization through the neuropeptide Y receptor subtype in several rat veins. 1268 92

The aim of this study was to investigate the synergism between neuropeptide Y and other vasoconstrictors (phenylephrine and serotonin) and which neuropeptide Y receptor subtype is responsible for the neuropeptide Y-induced potentiation. Exogenous neuropeptide Y (10 nM) potentiated alpha1-adrenoceptor-mediated (PE-induced) contraction in rat femoral artery permissively without its direct action, but not in the thoracic aorta. In contrast, neuropeptide Y produced no change in serotonin-induced contraction in both arteries. Increasing concentrations of neuropeptide Y caused dose-dependent potentiation of the phenylephrine-induced contraction in the femoral artery. This potentiation was blocked by a selective neuropeptide Y-Y1 receptor antagonist, BIBP3226 [(R)-N2-(diphenylacetyl)-N-[4-hydroxyphenyl)methyl]-argininamide] (1 microM). Semiquantitative reverse transcriptase polymerase chain reaction showed the selective expression of neuropeptide Y-Y1 receptor mRNA in the femoral artery. These findings indicated that the neuropeptide Y-induced selective potentiation of alpha1-adrenoceptor-mediated contraction is mediated through neuropeptide Y-Y1 receptor in rat femoral artery.
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PMID:Neuropeptide Y selectively potentiates alpha1-adrenoceptor-mediated contraction through Y1 receptor subtype in rat femoral artery. 1487 Oct 26

The action of neuropeptide Y (NPY) on food intake is of interest for the enhancement of growth of channel catfish (Ictalurus punctatus) for aquaculture. We sequenced 795 bp of complementary DNA (including 288 bp of open reading frame that encompassed the signal peptide, mature peptide, and carboxy-terminal peptide) from catfish brain NPY (GenBank accession number AF267164) and identified untranslated regions of the gene. We found high identity (88%-91%) of the amino acid sequence of the translated, mature protein with other fish NPYs. Using Northern blotting and reverse transcriptase polymerase chain reaction, we found NPY gene expression in the hypothalamus, myelencephalon, telencephalon, and optic tectum of the brain, but not the cerebellum or the pituitary gland. NPY expression was also found in immature ovary. Our results highlight the conserved nature of NPY in vertebrate systems, and the probes developed in this work will facilitate physiological and genetic studies of feeding and growth in channel catfish.
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PMID:Neuropeptide Y sequence and messenger RNA distribution in channel catfish (Ictalurus punctatus). 1496 73

The role of interneurons in neurovascular coupling was investigated by patch-clamp recordings in acute rat cortical slices, followed by single-cell reverse transcriptase-multiplex PCR (RT-mPCR) and confocal observation of biocytin-filled neurons, laminin-stained microvessels, and immunodetection of their afferents by vasoactive subcortical cholinergic (ACh) and serotonergic (5-HT) pathways. The evoked firing of single interneurons in whole-cell recordings was sufficient to either dilate or constrict neighboring microvessels. Identification of vasomotor interneurons by single-cell RT-mPCR revealed expression of vasoactive intestinal peptide (VIP) or nitric oxide synthase (NOS) in interneurons inducing dilatation and somatostatin (SOM) in those eliciting contraction. Constrictions appeared spatially restricted, maximal at the level of neurite apposition, and were associated with contraction of surrounding smooth muscle cells, providing the first evidence for neural regulation of vascular sphincters. Direct perfusion of VIP and NO donor onto the slices dilated microvessels, whereas neuropeptide Y (NPY) and SOM induced vasoconstriction. RT-PCR analyses revealed expression of specific subtypes of neuropeptide receptors in smooth muscle cells from intracortical microvessels, compatible with the vasomotor responses they elicited. By triple and quadruple immunofluorescence, the identified vasomotor interneurons established contacts with local microvessels and received, albeit to a different extent depending on interneuron subtypes, somatic and dendritic afferents from ACh and 5-HT pathways. Our results demonstrate the ability of specific subsets of cortical GABA interneurons to transmute neuronal signals into vascular responses and further suggest that they could act as local integrators of neurovascular coupling for subcortical vasoactive pathways.
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PMID:Cortical GABA interneurons in neurovascular coupling: relays for subcortical vasoactive pathways. 1548 13

Galanin is a 29-amino-acid peptide expressed in dorsal root ganglion (DRG) neurones and spinal dorsal horn neurones. It affects pain threshold and has developmental and trophic effects. Galanin acts at three G-protein-coupled receptors, galanin receptors (GalR1-3), each expressed in the DRGs as suggested by in situ hybridization and/or reverse transcriptase-polymerase chain reaction. The GalR2 knockout (-/-) mice permit studies on the contributions of this receptor subtype to the role of galanin at the spinal level. At 1 week after sciatic nerve transection (axotomy), there were 16-20% fewer neurones in intact and contralateral DRGs of -/- mice as compared with wild-type (WT) mice. In addition, a significant neurone loss (26% reduction) was found in the ipsilateral DRGs of WT mice, whereas no further neurone loss was seen in -/- mice. Expression of several peptides has been examined after axotomy, including galanin, neuropeptide Y and two of its receptors as well as substance P, and no significant differences were found between -/- and WT mice in either ipsi- or contralateral DRGs, respectively. After thermal injury and spinal nerve ligation, onset and duration of hyperalgesia in the injured paw were similar in GalR2-/- and WT animals. Recovery from spinal nerve ligation-caused allodynia had the same kinetics in -/- and WT animals. These data are in line with earlier observations from the peripheral and central nervous system, suggesting that galanin actions mediated by GalR2 subtype are of importance in neurodevelopment and neuroprotection.
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PMID:Sensory neuronal phenotype in galanin receptor 2 knockout mice: focus on dorsal root ganglion neurone development and pain behaviour. 1648 44

Intrauterine growth restriction (IUGR) is one of the major causes of short stature in childhood. Abnormalities in the growth hormone (GH) axis have frequently been observed in children who are born intrauterine growth restricted and GH treatment is effective to improve final height. However, the way that the GH axis is involved is not fully understood. Previously, when investigating the effect of IUGR on the central somatotrophic axis, a hypothalamic effect was discovered with elevated somatostatin and decreased neuropeptide Y mRNA expression levels, whereas serum GH and insulin-like growth factor I (IGFI) were unaltered. These findings were thought to indicate a hypothalamic alteration of the GH axis due to IUGR, probably to compensate pituitary output, thereby normalising peripheral values of GH and IGFI. Therefore, the present study aimed to evaluate the effect of IUGR on the pituitary GH axis in this rat model. Pups from rats that underwent bilateral uterine artery ligation at day 17 of pregnancy were studied. Pituitary glands were collected from 1-year-old offspring for quantitative measurements of GH, GH-receptor (GH-R), GH-releasing hormone receptor (GHRH-R), somatostatin receptor subtype 2 and 5, IGFI and IGFI receptor mRNA levels using a real-time reverse transcriptase-polymerase chain reaction. In addition, liver GH-R and IGFI mRNA expression levels were measured and a radioimmunoassay was performed to determine serum IGFI levels. In the IUGR rat, levels of pituitary GH, GH-R and GHRH-R relative gene expression (RGE) were increased. No differences were found in the RGE level of all other pituitary growth factors, liver GH-R and IGFI, and serum IGFI concentration between IUGR and control rats. The present data show that intrauterine growth failure leads to changes in the pituitary that might counterbalance the effects found previously in the hypothalamus.
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PMID:Pituitary mRNA expression of the growth hormone axis in the 1-year-old intrauterine growth restricted rat. 1686 82


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