UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuronal expression of the protooncogene c-fos may serve as a marker of neural activity. We previously examined brain sites upon which GH exerts an immediate early influence in rats and determined that the c-fos gene was transiently expressed in the hypothalamic periventricular nucleus (PeV) and arcuate nucleus (ARC) after recombinant human GH (rhGH) administration. As the distribution of c-fos messenger RNA (mRNA)-containing cells appeared to overlap with that of somatostatin (SS) neurons in both the PeV and ARC, we hypothesized that GH exerts a feedback effect on hypothalamic SS neurons. To extend this hypothesis, we characterized the neurons expressing the c-fos gene in response to rhGH administration in hypophysectomized rats. Adult male Wistar rats were hypophysectomized 10 days before use. After hypophysectomy, rats received daily sc injections of cortisone acetate (0.5 mg/kg BW) and L-T4 (20 micrograms/kg BW). Four international units (1.33 mg) of rhGH were given iv through an indwelling right atrial cannula. The vehicle was given to the control animals. Coronal sections of the hypothalamus were processed for in situ hybridization after rhGH or vehicle administration. To estimate the localization of neurons expressing the c-fos gene, the adjacent hypothalamic sections, 30 microns in thickness, were processed for hybridization histochemistry for SS, neuropeptide-Y (NPY), or GRF mRNA. In the ARC, the distribution of c-fos mRNA-containing cells appeared to overlap with that of NPY and partially with that of SS mRNA-containing cells, but it clearly differed from the distribution of GRF mRNA-containing cells. In the PeV, distribution of the cells expressing the c-fos gene was comparable to that of SS mRNA-containing cells. To further ascertain the distribution, hypothalamic sections, 6 microns in thickness, were processed by double label in situ hybridization using a 35S-labeled c-fos cRNA probe and a digoxigenin-labeled NPY or SS cRNA probe. In the ARC, 65% of the c-fos gene-expressing cells were NPY neurons. In the PeV, 60% of the c-fos gene-expressing cells were SS neurons. NPY is known to act within the hypothalamus and inhibit GH secretion via SS in rats, and the NPY neurons in the ARC have been shown to project to SS neurons in the PeV. Our findings suggest that the feedback effect of GH on the hypothalamus is mediated not only by SS neurons in the PeV, but also by NPY neurons in the ARC.
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PMID:Growth hormone induces expression of the c-fos gene on hypothalamic neuropeptide-Y and somatostatin neurons in hypophysectomized rats. 798 69

Intracerebroventricular (i.c.v.) injection of somatostatin (SS) or arginine-vasopressin (AVP) elicits barrel rotation (BR) in rats. To identify the potential neuron structures involved in this characteristic behavior, the regional expression of the c-fos gene in rat brain after i.c.v. injection of SS (10 micrograms) or AVP (1 micrograms) was examined by hybridization histochemistry. The c-fos expression could serve as a marker of neuronal activity and/or neural transmission. Following SS-induced BR, c-fos gene expression was observed in the lingula, uvula, nodulus, simplex, centralis, and culmen of the cerebellum, while following AVP-induced BR, c-fos gene expression was observed in the first four of the above-mentioned regions of the cerebellum, but not in the centralis or culmen. In these regions, the c-fos mRNA signals were observed on the granular layer. Expression of the c-fos gene was immediately and transiently induced and was not observed in rats in which BR was not evoked after SS or AVP injection. In both control rats and SS- or AVP-injected rats, the c-fos gene expression was induced in the piriform cortex and the flocculus of the cerebellum. The findings suggest that BR is a manifestation of behavior induced by massive transsynaptic activation of the granular cells in the cerebellum.
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PMID:Barrel rotation evoked by intracerebroventricular injection of somatostatin and arginine-vasopressin is accompanied by the induction of c-fos gene expression in the granular cells of rat cerebellum. 809 47

A cortical infarct of 2 mm diameter was obtained in the parietal cortex after a craniotomy, disruption of the dura mater and topical application of 3 M KCl. It has been shown previously that the presence of a small cortical infarct induces an increase in immediate early gene messenger RNA expression followed by an increase in neuropeptide and glutamic acid decarboxylase messenger RNA expression. Glutamate, acting at N-methyl-D-aspartate receptors, is held responsible for these changes, since they are blocked by pretreatment with dizocilpine. In the present study, we have analysed the consequences of the dramatic changes in messenger RNA expression on the level of immediate early gene products c-fos and zif 268, and on that of neuropeptides by using immunohistochemistry. After just 1 h, an increase in c-fos- and zif 268-like immunoreactivity is observed in the entire cortical hemisphere homolateral to the infarct, and is no longer detected after 6 h. An increase in cholecystokinin octapeptide-, substance P-, neuropeptide Y- and somatostatin-like immunoreactivity is observed in the entire cortical hemisphere homolateral to the infarct after three days, and is no longer detected after 30 days. To investigate if these dramatic increases in neuropeptide immunoreactivities may have functional consequences, we studied the level of cholecystokinin receptors by autoradiographic binding using [125I]cholecystokinin-8S and in situ hybridization for the detection of cholecystokinin-b receptor messenger RNA. A decrease in cholecystokinin binding sites and cholecystokinin-b receptor messenger RNA is observed in the entire cortical hemisphere homolateral to the infarct after three days, and is no longer detected after nine days. This study shows that a topical stimulation has diffuse effects, reaching regions far from the site of the lesion, and some of them are still strongly present after nine days. The increase in neuropeptide messenger RNAs is followed by an increase in the protein products of these genes, which may modify the neurotransmission. As a corollary to this, a decrease in cholecystokinin binding sites occurs. This may have further consequences on signal transduction pathways. This decrease in cholecystokinin binding sites is associated with a decrease in the cholecystokinin-b receptor messenger RNA, and this is the first example of a decrease in messenger RNA levels in this experimental model.
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PMID:Homolateral cerebrocortical changes in neuropeptide and receptor expression after minimal cortical infarction. 859 53

GH feeds back on the hypothalamus and regulates its own secretion. We have previously shown that systemic administration of GH induces expression of the c-fos gene, a marker of neuronal activity, on the hypothalamic neuropeptide Y(NPY) and somatostatin neurons in rats. We argued that if GH were to act directly on NPY neurons, NPY neurons should express the GH receptor (GHR) gene. To test this hypothesis, coronal sections of the medial basal hypothalamus from adult male Wistar rats were processed by double label in situ hybridization using a 35S-labeled NPY complementary RNA probe and a digoxigenin-labeled GHR complementary RNA probe. In the medial basal hypothalamus, NPY messenger RNA (mRNA) was observed in the arcuate nucleus (ARC) and the dorsomedial nucleus. The majority (95%) of NPY mRNA-containing cells in the ARC expressed the GHR gene, whereas no NPY mRNA-containing cells in the dorsomedial nucleus expressed the GHR gene. These findings suggest that NPY neurons in the ARC mediate the feedback effect of GH on the hypothalamus.
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PMID:Growth hormone receptor gene is expressed in neuropeptide Y neurons in hypothalamic arcuate nucleus of rats. 861 54

GH is thought to exert a short-loop feedback action on the hypothalamic somatostatin- and GH-releasing hormone (GHRH)-containing neurons. The direct actions of GH are mediated through GH receptors. In the male rat, few GHRH-containing neurons in the arcuate nucleus (ARC) appear to express the GH receptor messenger RNA (mRNA); however, some unidentified neurons near GHRH neurons do. Recent evidence suggests that neuropeptide-Y (NPY)-containing neurons, which are located near GHRH neurons in the ARC, are targets for GH action because treatment of rats with GH induces c-fos expression in these cells. We conducted two experiments to test the hypothesis that GH acts on NPY neurons in the ARC. First, we performed double-label in situ hybridization to determine whether NPY neurons in the ARC express GH receptor mRNA. Second, we investigated the possibility that GH regulates NPY mRNA expression by using in situ hybridization to compare ARC NPY mRNA levels among groups of normal (n = 7), hypophysectomized (n = 7), and hypophysectomized/rGH-treated (1.5 mg rat GH over 3 days; n = 6) rats. We found that most of the NPY-containing neurons in the ARC expressed GH receptor mRNA, whereas hypothalamic NPY neurons residing outside of the ARC did not. Furthermore, hypophysectomy significantly decreased NPY mRNA levels, and GH treatment restored the levels to those of the intact animals. We conclude that GH regulates the activity of NPY neurons in the ARC by a direct action on GH receptors that are expressed by NPY neurons. Whether the action of GH on NPY neurons in the ARC is related to the feedback control of GH secretion or some other physiological function remains to be determined.
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PMID:Regulation of hypothalamic neuropeptide-Y neurons by growth hormone in the rat. 862 6

Central glucoprivation evoked by the intracerebroventricular administration of 2-deoxy-D-glucose (2DG) induces eating and suppresses growth hormone (GH) secretion in rats. To elucidate the hypothalamic mechanism of these phenomena, the induction of c-fos gene expression was examined by in situ hybridization using rats with centrally administered 2DG. Autoradiography on X-ray film showed that c-fos gene expression was transiently induced in discrete hypothalamic regions; namely the paraventricular nucleus, arcuate nucleus (ARC), the surrounding regions of the third ventricle dorsal to the ARC, and the periventricular nucleus (PeV). The time course of the expression was different in these nuclei. Double-label in situ hybridization for c-fos mRNA and neuropeptide Y (NPY) or somatostatin mRNAs revealed that 20% of the NPY neurons in the ARC expressed the c-fos gene, while a small population of somatostatin neurons (6.1% in the ARC and 2.6% in the PeV) expressed the c-fos gene following 2DG administration. Since NPY is an orexigenic neuropeptide and has an inhibitory effect on GH secretion, the data suggest that the activation of a subpopulation of NPY neurons in the ARC contributes, in part, to the increased food intake and suppression of GH secretion after central glucoprivation evoked by 2DG.
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PMID:Central glucoprivation evoked by administration of 2-deoxy-D-glucose induces expression of the c-fos gene in a subpopulation of neuropeptide Y neurons in the rat hypothalamus. 875 Aug 90

Induction of c-fos mRNA and Fos was studied in the hilus and granular layer of the dentate gyrus at various times up to 24 h after single electroconvulsive stimulation (ECS) using in situ hybridization and immunocytochemistry. In both areas of the dentate gyrus, a prominent induction of c-fos mRNA and Fos was observed. Compared to the granular layer, however, c-fos mRNA and Fos in hilar cells reached maximum later and remained elevated considerably longer. Several neurochemically distinct populations of hilar neurons have been described, some of which contain neuropeptide Y (NPY) and/or somatostatin (SS). Using double-labelling immunocytochemistry, we examined to what extent Fos was induced in these hilar neurons after ECS. Although a minor population of non-NPY non-SS cells displayed Fos induction early after ECS, prolonged induction of Fos almost exclusively occurred in NPY or SS neurons. The Fos-immunoreactive NPY or SS neurons only amounted to about 50% of the total hilar population of NPY or SS neurons. The present observations suggest that a subpopulation of hilar NPY and SS neurons may be central to the actions of electroconvulsive seizures in the dentate gyrus.
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PMID:Prolonged induction of c-fos in neuropeptide Y- and somatostatin-immunoreactive neurons of the rat dentate gyrus after electroconvulsive stimulation. 878 3

Growth hormone-releasing hexapeptide (GHRP) stimulates GH secretion by acting on both the pituitary and the hypothalamus through a poorly understood mechanism. To reveal the hypothalamic action of GHRP, rat brains were processed for in situ hybridization for c-fos mRNA as a marker of neuronal activity after systemic administration of a newly developed GHRP, KP-102. Hypophysectomized adult male Wistar rats were administered KP-102 through an indwelling right atrial cannula. KP-102 treatment was accompanied by transient expression of the c-fos gene selectively in the ventromedial and ventrolateral regions of the arcuate nucleus (ARC). The distribution of c-fos gene-expressing cells overlapped that of GRF mRNA-containing neurons in the ventrolateral region on adjacent sections, whereas few c-fos mRNA signals were detected in the dorsomedial region where somatostatin mRNA signals were localized. To confirm this observations, hypothalamic sections were subjected to double-label in situ hybridization. Twenty-three percent of c-fos mRNA-containing cells were GRF neurons, comprising 20% of the GRF neurons in the ARC. The remaining c-fos mRNA containing cells were unidentified. KP-102 thus appears to act on a subpopulation of GRF neurons and unidentified cells in the ARC to stimulate GH secretion.
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PMID:The growth hormone-releasing peptide KP-102 induces c-fos expression in the arcuate nucleus. 880 23

The neuroendocrine regulation of pulsatile growth hormone (GH) secretion involves the reciprocal interactions between growth hormone-releasing hormone (GHRH)- and somatostatin-containing neurones, residing primarily in the hypothalamic arcuate nucleus (ARC) and the periventricular nucleus (PeN), respectively. Considerable evidence supports the concept that GH itself participates in the regulation of its own rhythmic secretion through a reciprocal feedback on GHRH and somatostatin neurones. The direct actions of GH are mediated through GH receptors, and in the PeN, the majority of somatostatin neurones express this receptor. GH induces the expression of the immediate early gene c-fos in the ARC; however, few GHRH residing in the ARC express the GH receptor, suggesting that the action of GH on GHRH cells must be indirect through another population of unidentified cells. NPY neurones express c-fos in response to GH, and preliminary results suggest that NPY neurones in the ARC express the GH receptor. These observations suggest that NPY neurones play a physiological role in the feedback of regulation of GH secretion.
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PMID:Role of NPY neurones in GH-dependent feedback signalling to the brain. 880 21

Activation of both calcium and AMP-dependent regulatory pathways promotes survival of cerebellar neurons in vitro. Complex cellular programs such as survival must involve precise genetic responses. We show here, at the genomic level, that depolarization potentiates AMP-driven transcription of a variety of genes including the c-fos and c-jun proto-oncogenes, and the gene for somatostatin, proenkephalin and nerve growth factor. We used a reporter gene driven by the minimal AMP-responsive element (TGACGTCA) as a model system for studying this class of genes. In primary neurons, this reporter construct is co-activated in a synergistic manner by forskolin and KCl. We show that, in contrast to AMP, calcium-driven transcription does not require functional AMP-dependent protein kinase. Thus, when calcium and AMP levels are increased, these two second messengers stimulate transcription through different kinases which converge at the level of the AMP-responsive element. In addition, lower levels of intracellular free calcium can potentiate AMP-dependent transcription. This effect results from increased cyclic AMP accumulation and is strictly mediated by the AMP/AMP-dependent protein kinase pathway. In summary, low and high calcium concentrations potentiate AMP-dependent transcription via distinct mechanisms. Low calcium increases AMP production, whereas high calcium activates a non-cyclic AMP-dependent protein kinase, which in turn synergizes with AMP-activated transcription. These distinct mechanisms are likely to operate under specific physiological conditions within the neuronal network.
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PMID:Fine tuning of calcium entry into neurons regulates adenosine 3',5'-monophosphate-dependent transcription by several distinct mechanisms. 884 67

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