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)

Combined immunohistochemical labelling for neurons containing growth hormone (GH) releasing factor (GRF) or somatostatin and single labelling immunohistochemistry combined with Fluorogold retrograde transport labelling were used to examine whether somatostatin or GRF neurons might be reciprocally innervated. Occasional somatostatin-immunoreactive neurons in the periventricular preoptic area were found to be closely approached by GRF-immunoreactive fibres, providing possible evidence of scant innervation of somatostatin neurons by GRF cells. In contrast, many GRF-immunoreactive neurons in the arcuate nucleus appeared to have somatostatin-immunoreactive fibres closely applied to their perikarya suggesting that GRF neurons might be innervated by somatostatin cells. Combined retrograde tracing and fluorescence immunohistochemistry revealed few somatostatin-immunoreactive neurons doubly labelled following injections of Fluorogold in the basal hypothalamus. Occasional GRF-immunoreactive neurons in the basal hypothalamus were doubly labelled following PO/AHA injections of Fluorogold. Numerous somatostatin-immunoractive perikarya were observed in the periventricular arcuate region in colchicine-pretreated animals. We conclude that GH-regulating neurons do not have strong reciprocal innervation. The innervation of GRF neurons by somatostatin fibres may be derived from local somatostatin neurons.
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PMID:Hypothalamic interconnections of somatostatin and growth hormone releasing factor neurons. 257 37

Possible effects of GRF on somatostatin neurons and of somatostatin on GRF neurons were examined by measuring the effects of localised intracerebral injections of these peptides on growth hormone (GH) secretion. Serial GH concentrations were measured in plasma in unanaesthetized male rats chronically prepared with venous and intracerebral cannulae, before and after treatment with bilateral intracerebral injections of somatostatin or GRF in the preoptic anterior hypothalamic area (PO/AHA) and medial basal hypothalamus. Injections of 0.1 and 1 nmol of GRF in medial basal hypothalamus or 10 nmol somatostatin in the PO/AHA, respectively, had stimulatory or inhibitory effects on GH, which were assumed to be due to diffusion of the peptide from the injection site to the median eminence and pituitary gland. Injection of lower doses of somatostatin around GRF neurons in the medial basal hypothalamus were without significant effect on secretion of GH, but 0.1 nmol somatostatin in the PO/AHA resulted in an increase in GH concentrations from 128 +/- 61 to 524 +/- 103 ng/ml, p less than 0.02. Injections of GRF in lower doses amongst somatostatin neurons in the PO/AH or amongst GRF neurons in the medial basal hypothalamus were both without effect on GH secretion. We conclude that somatostatin may stimulate GH secretion by an effect on or close to somatostatin neurons in the PO/AHA. Somatostatin, though present in terminals on GRF neurons, is without effect at this site in our model. Furthermore, we have been unable to demonstrate any significant intrahypothalamic effect of GRF on GH regulation.
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PMID:Intrahypothalamic actions of somatostatin and growth hormone releasing factor on growth hormone secretion. 257 38

The in vitro effects of human growth hormone releasing factor (hGRF, 1-44) were studied in somatotroph-enriched cultures (75-85%) obtained from adult male rat pituitaries. Cells perifused with hGRF showed an up to 800% increase in growth hormone (GH) release over basal values in a dose-dependent manner. Calcium current blockers (5 mM of Co2+, Ni2+ or Cd2+) completely inhibited this stimulating effect but sodium-free (choline) medium did not. Using a single-intracellular-electrode recording technique, it was found that hGRF induced a dose-dependent depolarizing response concomitant with a decrease in membrane resistance in 38% of the cells recorded (98 of 258 cells). The reversal potential of this response was close to -40 mV. This depolarizing response was recorded in both excitable and unexcitable cells with no marked difference. Co2+ and Ni2+ (5 mM) completely and reversibly inhibited the membrane response to hGRF. Application of hGRF and somatostatin (SRIF), a hormone that inhibits GH release, to the same cell cultures showed the existence of two subpopulations: one was responsive to both hGRF and SRIF (53%, n = 62), another was only responsive to SRIF (47%, n = 62). Human GRF did not affect prolactin release and did not modify the electrical properties of cells responding to dopamine and therefore considered as lactotrophs. These results suggest that (1) hGRF leads to an increase in growth hormone release and a modification of membrane electrical properties by means of an extracellular Ca2+-dependent pathway, and (2) according to their responses to SRIF and hGRF, there are at least two subpopulations of somatotrophs.
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PMID:Electrophysiological responses of rat pituitary cells in somatotroph-enriched primary culture to human growth-hormone releasing factor. 257 14

A novel pituitary protein "7B2" was secreted by GH1 cells. The secretion of 7B2 was increased in the presence of human GRF in a dose-responsive manner. In contrast, a somatostatin analog, SMS 201-995, revealed the inhibitory effects on the basal- and GRF-induced secretion of 7B2 at the concentration of 10(-7) M. These findings suggest that 7B2 is a secretory protein of rat GH1 cells under certain conditions.
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PMID:Effect of GRF and somatostatin on 7B2 secretion by rat GH1 cells. 257 51

GH secretion and mRNA levels were measured in cultured cells obtained from six human pituitary somatotroph tumors to investigate their hormonal and intracellular regulation. The responses were variable between tumors, but, in general, mRNA levels were less responsive than GH release to in vitro manipulation. GH-releasing factor [GRF-(1-29) amide; 10 nM] increased GH release and mRNA levels in three of four tumors tested to 30-97% above control values, but the fourth tumor was unresponsive. Somatostatin (1 microM) inhibited GH release significantly in four of the six cases, to 35-79% of control levels, but had no inhibitory effect on GH mRNA accumulation, in contrast to earlier studies on rat pituitary tissue. Bromocriptine (100 nM) likewise inhibited GH release (50-75% of control), but not GH mRNA levels, in the four tumors tested. Forskolin (10 microM; used to activate adenylate cyclase) stimulated GH release and mRNA levels in the two cases that responded most clearly to GRF, but had no significant effect in the other tumors; however, the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (100 nM) had no consistent effect on mRNA levels despite stimulating secretion in four of six cases. Thus, there was considerable variation in responses among the tumors tested; however, the responsiveness to GRF was approximately paralleled by that to forskolin, consistent with the suggestion that adenylate cyclase activity and responsiveness are variable among these tumors. Furthermore, the divergent effects of somatostatin on GH release and mRNA suggest uncoupling between its receptor and transcriptional regulatory mechanisms.
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PMID:Regulation of growth hormone secretion and messenger ribonucleic acid accumulation in human somatotropinoma cells in vitro. 277 32

Atrial natriuretic factor (ANF) binding sites in adult rat exocrine pancreas were studied by autoradiography using slide-mounted frozen tissue sections with mono-iodinated ANF (101-126) as the tracer. Radiolabel was displaced by unlabeled atrial peptide (IC50 = 2 X 10(-11) M). High specific labeling was found in pancreatic acini. The presence of endogenous ANF has also been demonstrated in the exocrine pancreas by immunocytochemistry on ultra-thin sections obtained by cryoultramicrotomy. ANF-like immunoreactivity was found in acinar and centro-acinar cells as well as cells of the intercalated duct. For these cells, immunostaining was observed at the plasma membrane level, in the cytoplasm and nucleus. In the cytoplasm, ANF-like immunoreactivity was observed in the cytoplasmic matrix, mitochondria, and zymogen granules. In the nucleus, ANF-like immunoreactivity was distributed in the vicinity of the heterochromatin region primarily in the euchromatin. It was also detected in the plasma membrane of microvilli of acinar and duct cells, and in the lumen of secretory ducts. In centro-acinar cells, the reaction product was also found sparsely at the nuclear envelope. No immunoreactivity was observed when anti-human ANF serum preincubated with rat ANF was used. No modifications were observed when this antiserum was preincubated with heterologous peptides (NPY, CRF, GRF, TRH, somatostatin). These data provide autoradiographic evidence of ANF binding sites, indicate the presence of this peptide in acinar and centro-acinar cells as well as cells of the intercalated duct, and immunocytochemical evidence for the internalization of endogenous ANF by exocrine pancreas.
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PMID:Atrial natriuretic factor and exocrine pancreas: autoradiographic localization of binding sites and ultrastructural evidence for internalization of endogenous ANF. 281 60

Regulation of adenohypophyseal hormone secretions has been shown to involve cyclic AMP production, modulation of phosphatidyl inositol diphosphate breakdown and Ca2+ mobilization. Various neurohormone receptors are positively or negatively coupled to adenylate cyclase activity in anterior pituitary cells. The effects of these neurohormones on adenylate cyclase activity are consistent with the effect on hormone secretions, suggesting that modulation of the enzyme activity is actually involved in the regulation of adenohypophyseal secretions. Thus DA inhibits, whereas VIP stimulates adenylate cyclase activity of the same cell type, which, according to the effect of these neurohormones on prolactin secretion, appear to be lactotrophs. On the other hand, SRIF inhibits, whereas GRF stimulates the adenylate cyclase activity of another cell type, namely somatotrophs, whereas CRF appears to act on a third cell type, corticotrophs. Peripheral hormones have been shown to modulate the sensitivity of anterior pituitary cells to these neurohormones. Estradiol long-term treatment has an anti-dopaminergic effect on prolactin secretion. The steroid also suppresses the dopamine inhibition of adenylate cyclase. This effect appears selective to the DA inhibition, since AII inhibition of the enzyme is only partially reduced, whereas the somatostatin inhibition is markedly increased. Peripheral hormones seem to affect the sensitivity of adenohypophyseal cells not only by modulating the number of receptors for a given neurohormone but also by interfering with the coupling mechanisms of these receptors. AII and DA inhibit the adenylate cyclase activity of lactotroph cells. The prolactin stimulation induced by angiotensin is not consistent with the effect of the peptide on adenylate cyclase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple coupling of neurohormone receptors with cyclic AMP and inositol phosphate production in anterior pituitary cells. 282 May 13

Radioimmunoassays of brain extracts have shown that several peptides occur in high concentrations in the CNS. The releasing-factor peptides TRF, LRF, somatostatin, CRF and GRF have the highest concentration in the hypothalamic extracts. High levels of somatostatin, CCK octapeptide, neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) are found in cortical extracts. Substance P, CCK, NPY, and enkephalins are present in high concentrations in basal ganglia and mesolimbic areas. Pharmacological doses of these peptides result in several behavioural and vegetative effects. Immunocytochemical studies show that the CNS peptides are localised in neurones and in synaptic vesicles. In vitro studies with brain tissues show that peptides are capable of modifying the ongoing classical neurotransmission. In depressive patients several neuropeptides (CCK, CRF and NPY) have been shown to have low CSF levels. Patients dying of senile dementia have low cortical levels of somatostatin, CRF and substance P. In schizophrenic patients CCK peptides have shown to improve some symptoms. At present the therapeutic potentials of peptides are poorly known. More studies are required to understand their role in neurotransmission and related pathological states.
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PMID:Peptides and neurotransmission in the central nervous system. 282 29

Thymosin fraction 5 (TF5) is a partially purified extract of bovine thymus containing 40-60 peptides. In addition to its well documented immunopotentiating effects, TF5 reportedly modulates the secretion of some hypothalamic peptides and pituitary hormones. In this study, TF5 (10-100 micrograms/ml) stimulated PRL release from normal, MtTW15, and 7315a cells and GH release from normal and MtTW15 cells, but had no apparent effect on LH release. No changes in intracellular cAMP or cGMP levels could be correlated with these responses. Stimulation of PRL release from perifused normal anterior pituitary cells was rapid, sustained, and concentration related. Although it had no apparent effect on normal prelabeled anterior pituitary cells with respect to 45Ca2+ efflux, the calcium channel blocker D-600 inhibited TF5-mediated hormone release from these cells. Additive increases in TRH-stimulated PRL release and GRF-stimulated GH release by TF5 suggested independent mechanisms of action. Dopamine (500 nM) blocked TF5-stimulated PRL release, but somatostatin (10-100 nM) had no effect on TF5-stimulated PRL or GH release. TF5 failed to affect either basal or TRH-induced polyphosphoinositide hydrolysis. Perifused normal anterior pituitary cells prelabeled with [3H]arachidonate responded to TF5 treatment with a liberation of radioactive arachidonate and/or its metabolites. BW755c, an inhibitor of all known catabolic pathways of arachidonic acid, blocked the ability of TF5 to stimulate PRL and GH release. Reversed phase HPLC separation of TF5 into five fractions resulted in two fractions that exhibited hormone-releasing activity. These data suggest that TF5 stimulates pituitary hormone release through a mechanism different from that ascribed to TRH or GRF. The stimulus-secretion coupling mechanism involves neither polyphosphoinositide hydrolysis nor cAMP generation, but appears to be dependent on the generation of arachidonate metabolites.
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PMID:Thymosin fraction 5 stimulates prolactin and growth hormone release from anterior pituitary cells in vitro. 282 78

Human pancreatic growth hormone-releasing factor (GRF-44-NH2) stimulated growth hormone (GH) secretion and intracellular cyclic AMP levels in cultured pituitary cells from both sheep and rat. Somatostatin (SRIF), over a wide range of doses and time, showed no significant effect on the elevated cyclic AMP levels in sheep cells, but did block the GH release in a dose-dependent manner. In rat cells, however, SRIF inhibited GRF-stimulated cyclic AMP levels by 75% maximum (still 8-fold greater than the basal levels) and GH release to almost half the basal value. We conclude that somatostatin inhibits GRF-elevated cyclic AMP levels in rat pituitary cells but not in sheep cells.
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PMID:Effects of growth hormone-releasing factor and somatostatin on growth hormone secretion and cellular cyclic AMP levels. Cultured ovine and rat anterior pituitary cells show markedly different responses. 285 5


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