Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies were designed to assess whether a decline in pituitary response to growth hormone-releasing factor (GRF) contributes to the decline in amplitude of growth hormone (GH) pulses with age. Atrial cannulated young (3-4 months), middle-aged (12-14 months) and old (20-22 months) Fischer 344 male rats were anesthetized with pentobarbital to suppress pulsatile release of GH. One hour later, animals were injected with hpGRF(1-44) (10 micrograms/kg) and blood samples were removed at 0, 5, 10, 20, 40 and 80 min. Animals were then passively immunized with somatostatin antiserum and hpGRF(1-44) was reinjected. Samples were removed at the time intervals previously described. In response to 10 micrograms/kg GRF, plasma GH in young and middle-aged animals increased to 921 +/- 105 and 866 +/- 126 ng/ml, respectively, at 10 min and declined. In old animals, GH concentrations only increased to 654 +/- 80 ng/ml (p less than 0.05 compared to young rats). This represents a 28% reduction in the peak GH response to GRF. Despite passive immunization with somatostatin antiserum, the peak GH response to a second injection of GRF was diminished in all age-groups. However, integration of the area under the response curve indicated that GH secretion was similar in young and old animals during the 80-min sampling period after somatostatin antiserum. In another study, diethyldithiocarbamate (DDC; 250 mg/kg, i.v.), a dopamine-beta-hydroxylase inhibitor, was used to inhibit pulsatile GH release. One hour later, animals were injected with hpGRF(1-44) (50 micrograms/kg, i.v.) and blood samples were removed as previously described.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Growth hormone releasing hormone induced release of growth hormone in aging male rats: dependence on pharmacological manipulation and endogenous somatostatin release. 284 May 97

The role of prostaglandins (PGs) in the physiological secretion of the adenohypophyseal hormones, growth hormone (GH) and thyrotropin (TSH), in the unanesthetized, freely behaving male rat was investigated using pharmacological agents. Confirming previous observations, PG synthesis-inhibiting drugs, salicylate and indomethacin (INDO), reduced GH and TSH secretion. Another PG synthesis-inhibiting drug, acetaminophen, also reduced GH and TSH secretion. Antisomatostatin serum administered to INDO-treated rats indicated that somatostatin has a relatively small role in the GH and TSH suppression caused by PG synthesis inhibitors. Stimulation of GH secretion by the alpha 2-adrenergic receptor agonist, clonidine, and by morphine was similar in control and INDO-treated rats whereas PGE2 evoked a significantly greater release of GH in INDO- than in DDC- (dopamine beta-hydroxylase inhibitor-)treated rats. Stimulation of TSH secretion was similar in response to thyrotropin-releasing hormone (TRH) in INDO-treated and control rats and was also similar in response to PGE2 in INDO- and DDC-treated rats. However, clonidine evoked a significantly greater rise in TSH secretion in control than in INDO-treated rats. These results confirm the observation that PGs are important in physiological GH and TSH secretion in the rat and suggest that PGs are involved in GH secretion by interaction proximally to the adrenergic synapse on growth hormone-releasing factor (GRF) neurons and are involved in TSH secretion by interaction postsynaptically to the adrenergic synapse on TRH neurons.
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PMID:Endogenous prostaglandins affect growth hormone and thyrotropin release at a hypothalamic, not a pituitary level. 650 67

A variety of neuropeptides, such as TRH, somatostatin, VIP, Substance P, neurotensin, CCK, gastrin, and opioid peptides, alter secretion of GH and PRL from the pituitary. These actions differ according to the route of administration or with experimental conditions, especially anesthesia. Among these peptides, the most consistent results have been obtained with opioid peptides, which stimulate GH and PRL release. Both beta-endorphin and enkephalins are capable of stimulating GH and PRL release in anesthetized and unanesthetized, freely moving rats. The effect is blocked by naloxone, an opiate receptor antagonist. GH secretion induced by opioid peptides seems to be mediated by an alpha-adrenergic mechanism, since treatment with DDC and fusaric acid, which are dopamine-beta-hydroxylase inhibitors, reserpine, and phenoxybenzamine which is an alpha-adrenergic blocking agent, blunted GH secretion. However, pimozide, a dopamine receptor antagonist, and propranolol, a beta-adrenergic blocking agent, were without effect. On the other hand, basal PRL secretion was augmented by pimozide, suggesting the possible involvement of dopamine. It is also possible that serotonin is involved in the GH and PRL release induced by opioid peptides. The physiological significance of opioid peptides in regulating GH and PRL secretion is still unclear. Contradictory results (12,25) have been obtained concerning the effect of naloxone on basal or stimulated GH and PRL secretion in rats, monkeys and humans when tested by the continuous blood sampling method, which rules out the erroneous evaluation of results caused by episodicity of plasma hormone levels. Further studies should clarify the physiological role of opioid peptides in regulating pituitary function.
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PMID:Effect of CNS peptides on hypothalamic regulation of pituitary secretion. 701 Sep 47

The bed nucleus of the stria terminalis (BNST) is a complex integrative centre in the forebrain, composed of multiple sub-nuclei, each with discrete populations of neurons. Progress in understanding BNST function, both in the adult and during postnatal maturation, is dependent upon a more complete characterization of neuronal phenotypes in the BNST. The aim of the current study was to define the molecular phenotype of one postnatal BNST neuronal population, in order to identify molecular factors that may underlie both (protein marker-related) immaturity, and secondly, the transience of this phenotype. This BNST population was originally identified by high, but transient expression of the EGR1 transcription factor (TF) in postnatal rat lateral intermediate BNST (BNSTLI). The current results confirm a high level of Egr1 activation in postnatal day 10 (PN10) male BNSTLI that is lost at PN40, and now demonstrate a similar pattern of transient activation in female brains. Apparent cellular immaturity in this population, as indicated by low levels of the adult neuronal marker NeuN/RBFOX3, was found to be uncorrelated with both key neuronal regulator protein expression (SOX2 and REST), and also RBFOX2 protein levels. The BNSTLI neurons have a partial catecholaminergic phenotype (tyrosine hydroxylase-positive/dopa decarboxylase-negative; TH+ve/DDC-ve) that is lost at PN40. In contrast, the co-expressed neuropeptide, somatostatin, is maintained, albeit at lower levels, at PN40. The transcriptional basis of the transient and partial catecholaminergic phenotype was investigated by analysing TFs known to maintain adult dopaminergic (TH+ve/DDC+ve) neuronal phenotypes. The BNSTLI neurons were shown to lack forkhead TFs including FOXA1, FOXA2 and FOXO1. In addition, the BNSTLI neurons had low, primarily cytoplasmic, expression of NR4A2/NURR1, an orphan nuclear receptor that is critical for adult maintenance of midbrain dopamine neurons. These results detail the molecular features of an immature neuronal phenotype, and reveal TF deficiencies that may underlie postnatal transience of the phenotype.
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PMID:Molecular phenotyping of transient postnatal tyrosine hydroxylase neurons in the rat bed nucleus of the stria terminalis. 2841 31