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)

We have used antisera specifically directed against Met-enkephalin (met-ENK), somatostatin (SOM), substance P (SP), and vasoactive intestinal peptide (VIP), to study the development of neurons containing these peptides in the foregut of the chick. All four peptides were detected early in ontogeny, at 4 to 9 days of incubation (d.i.), and were localized primarily to cell bodies in the primitive myenteric plexus. There were differences in the times at which they were first detected and in the sequence of their appearance in the proventriculus, gizzard, and duodenum. The differentiation of these peptidergic neurons in the duodenum was examined in some detail. Cell bodies containing these peptides were first detected in the primitive myenteric plexus at 5 to 7 d.i. and increased in number from 7 to 11 d.i. Processes containing varicosities became prominent between 11 and 13 d.i. VIP was the first of the peptides to appear in the submucosal plexus and was found in more proximal regions of the duodenum at 5 d.i. Shortly thereafter, SOM- and SP-containing cell bodies were seen; met-ENK-containing cell bodies were never detected in the submucosal plexus. At 13 d.i., the circular smooth muscle contained a number of VIP-immunoreactive and a smaller number of SOM-immunoreactive processes. met-ENK- and SP-immunoreactive processes appeared in the circular smooth muscle between 17 and 21 d.i.; VIP- and SP-immunoreactive processes appeared in the mucosal plexus at 17 to 21 d.i. Our results suggest that neuropeptides appear very early in the ontogeny of enteric neurons, at the same time or even before cholinergic and serotonergic neurons express their phenotypes. These findings argue against a sequential developmental order in which peptidergic neurons appear after those containing acetylcholine and serotonin.
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PMID:The development of peptidergic neurons in the foregut of the chick. 619 17

Twenty-two endocrine carcinomas of the skin were examined immunohistochemically for the presence of several polypeptides and serotonin. Eight tumors contained one or more polypeptides. Occasional cells containing calcitonin were found in several tumors. Rare cells with substance P, somatostatin, and ACTH were present in only one tumor each. None of the patients presented a clinical syndrome associated with any of these polypeptides. Met-enkephalin and serotonin were negative in all tumors. The lack of demonstration of met-enkephalin in these tumors makes their relationship to the Merkel cell uncertain.
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PMID:Immunohistochemical studies in endocrine carcinoma of the skin. 620 32

The colocalization of acetylcholine (ACh) and neuropeptides (e.g., substance P and enkephalins) in the splanchnic nerve terminals suggests that these compounds might interact to modulate adrenal catecholamine release. Use has been made of primary monolayer and suspension cultures of bovine adrenal chromaffin cells to investigate postsynaptic receptor interactions between acetylcholine and a number of neuropeptides endogenous to the adrenal medulla and splanchnic nerve. The cells have both nicotinic and muscarinic acetylcholine receptors, but only the nicotinic receptors stimulate catecholamine release. Substance P, somatostatin, and the enkephalins all produced an inhibition of the ACh-evoked secretion of catecholamines, but their potency ranged over 100-fold. Substance P was the most potent with a mean inhibitory concentration (IC50) of 10(-6) M and Leu-enkephalin the least potent with an IC50 greater than 10(-4) M. These pharmacological effects were monitored conveniently by measuring the release of [3H]norepinephrine preloaded into the cells or alternatively, "on-line" by measuring ATP released into an incubation medium containing luciferin and firefly tail extract (luciferase). Of interest, the endogenous enkephalin heptapeptide (Met-enkephalin Arg6-Phe7) and "big" Met-enkephalin (BAM- 22P ) were some 100-fold more effective than Leu- or Met-enkephalin at inhibiting the nicotinic secretin of catecholamines, suggesting that a unique opiate receptor may be involved. Substance P had two distinct actions on the nicotinic response: (1) substance P inhibited acetylcholine-induced release of catecholamines; and (2) substance P protected against acetylcholine-induced desensitization of catecholamine release. With regard to (1), substance P inhibited the secretion of catecholamines and ATP evoked by acetylcholine or nicotine but not that evoked by K+ or veratridine, nor did substance P by itself affect secretion. Substance P appeared to interact with a regulatory site on the acetylcholine receptor - ionophore complex. Substance P receptors on chromaffin cells have similar structural requirements for activation as do substance P receptors in other substance P responsive tissues. With regard to (2), substance P (greater than 5 X 10(-6) M) completely protected against desensitization of catecholamine release produced by acetylcholine (greater than 10(-4) M) or nicotine (greater than 2.5 X 10(-6) M) with no effect on K+-induced desensitization.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Receptors and receptor modulation in cultured chromaffin cells. 620 33

beta-Endorphin, Met-enkephalin, substance P, and somatostatin concentrations were evaluated in the hypothalami of rats treated either acutely or chronically (15 days) with sodium valproate, diphenylhydantoin, phenobarbital, or ethosuximide. All of these drugs, with the exception of ethosuximide, induced significant decreases in beta-endorphin concentrations after acute treatment, while only sodium valproate induced a decrease after chronic treatment. The acute and chronic effects of sodium valproate were also produced by aminooxyacetic acid, an inhibitor of gamma-aminobutyric acid (GABA) transaminase, while another GABA transaminase inhibitor, ethanolamine-O-sulphate, and THIP, a GABA receptor agonist, were effective after acute administration. Metenkephalin, substance P, and somatostatin concentrations were never affected by the drugs used. The present results, indicating that antiepileptic agents specifically decrease beta-endorphin concentrations, seem to correlate well with the capacity of these agents to blunt the epileptic activity of the peptides tested. Moreover, our data suggest that GABA may be involved in the anticonvulsant-induced reduction of beta-endorphin concentrations.
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PMID:Antiepileptic agents affect hypothalamic beta-endorphin concentrations. 620 24

Intraventricular injections of beta-endorphin, gamma-endorphin and alpha-endorphin were demonstrated to reduce isolation-induced distress vocalization on 2-4 day old chicks in a dose response manner at doses as small as 12.5 picomoles (pmol). beta-Endorphin was more potent than the other peptides and morphine, while Met-enkephalin was without effect. However, the D-Ala2 substituted form of Met-enkephalin was as potent as morphine. None of the opioid peptides was effective when injected peripherally in doses of 400 pmol/g body weight. Extension of the interval between injection and behavioral observation from 4 minutes eliminated the ability of alpha- and gamma-endorphin to reduce the peeps. Specificity of the opioid effect was determined by testing intraventricular injections (200 pmol) of 9 other endogenously found peptides. Somatostatin, vasoactive intestinal peptide, and human pancreatic peptide reduced the vocalizations modestly, while alpha-MSH reliably increased them.
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PMID:The pharmacology of endorphin modulation of chick distress vocalization. 620 36

The release of Met-enkephalin immunoreactive material (ME-IR) from rat spinal slices was measured in vitro. This release increased about 4 fold in response to the addition of K+ ions. K+-evoked release of ME-IR was Ca++ dependent. Veratridine, a depolarizing agent, also stimulated the release of ME-IR. Veratridine-induced ME-IR release was completely prevented by tetrodotoxin (TTX), a Na+ channel blocker. Somatostatin (SRIF) inhibited both basal and K+-evoked release of ME-IR at 10(-7) M. Substance P had a similar effect although higher concentrations were needed. gamma-Aminobutyric acid (GABA) and neurotensin (NT) did not affect the basal release but slightly decreased K+-evoked release at 10(-5) M. Serotonin (5-HT) and noradrenaline (NA), did not affect ME-IR release. These results suggest that some of the neuropeptides present in the spinal cord, especially SP and SRIF, may be potent modulators of ME-IR release at the spinal level.
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PMID:Neuropeptidergic inhibitory regulation of Met-enkephalin immunoreactive material release from rat spinal cord in vitro. 620 87

Receptors for porcine vasoactive intestinal peptide have been characterized in isolated epithelial cells of rat ventral prostate. The interaction of 125I-labelled VIP with cells was rapid, reversible, specific, saturable and dependent on temperature. Degradation of peptide and receptors was minimized at 15 degrees C. At apparent equilibrium, the binding of 125I-labelled peptide was competitively inhibited by native VIP in the 1 X 10(-10)-10(-7)M range concentration. The binding data were compatible with the existence of two classes of receptors: a high-affinity class with a Kd = 4.0 nM and a low binding capacity (0.12 pmol VIP/mg cell protein), and a low-affinity class with a Kd = 17.8 nM and a high binding capacity (1.6 pmol VIP/mg cell protein). Chicken VIP and porcine secretin exhibited a 7-fold higher and a 7-fold lower affinity than porcine VIP for binding sites, respectively. Glucagon, Leu-enkephalin, Met-enkephalin and somatostatin were ineffective. The presence of high-affinity receptors for VIP together with previous reports on the occurrence of VIP-containing neurones innervating the male genitourinary tract strongly suggest that this peptide may be important in the physiological regulation of the functions of prostatic epithelium.
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PMID:Receptors for vasoactive intestinal peptide on isolated epithelial cells of rat ventral prostate. 631 51

Vasoactive intestinal peptide (VIP) has been shown to increase cyclic AMP content in isolated epithelial cells of rat ventral prostate. The stimulatory effect of VIP was dependent on time and temperature and was potentiated by a phosphodiesterase inhibitor. At 15 degrees C, the response occurred in the 1 X 10(-10)-10(-7)M range of VIP concentrations. Half-maximal stimulation of cellular cyclic AMP was obtained at 1.4 nM and maximal stimulation (3-fold basal level) at about 100 nM VIP. Chicken VIP and porcine secretin were agonists of porcine VIP but exhibited a 2-times higher and a 170-times lower potency, respectively. A high concentration (1 X 10(-6)M) of glucagon, somatostatin, neurotensin, substance P, Met-enkephalin or Leu-enkephalin did not modify cAMP levels. The finding of a VIP-stimulated cAMP system in rat prostatic epithelial cells together with the previous characterization of high-affinity receptors for VIP in the same cell preparation, as well as the presence of VIP-containing neurones innervating the male genitourinary tract, strongly suggest that VIP may be involved in prostatic growth regulation and function.
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PMID:Cyclic AMP-stimulating effect of vasoactive intestinal peptide in isolated epithelial cells of rat ventral prostate. 631 52

The presence of cells with peptidergic immunoreactivity in neural crest cell cultures and the influence of fibronectin on their in vitro differentiation were evaluated by indirect immunostaining. Met-enkephalin-like immunoreactive and somatostatin-like immunoreactive cells were observed. Met-enkephalin-like immunoreactive cells resembled endocrine cells. A variety of morphologies was observed in the cells with somatostatin-like immunoreactivity: cells without processes which looked like endocrine cells, multipolar cells with long varicose processes resembling sympathetic neurons, and bipolar cells which were similar to sensory neuroblasts. Differentiation of both types of peptidergic cells was promoted by adding fibronectin to the culture medium. The results suggest that neural crest cell cultures may become a valuable experimental system with which to study the early development of peripheral peptidergic neurons and endocrine cells.
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PMID:Fibronectin-regulated methionine enkephalin-like and somatostatin-like immunoreactivity in quail neural crest cell cultures. 639 23

Under control conditions, superfused slices of the dorsal half of the lumbar enlargement from adult rats released Met-enkephalin-like material (MELM) that behaved as authentic Met-enkephalin under two different chromatographic procedures (Bio-gel filtration, HPLC). MELM release increased markedly on exposure of slices to batrachotoxin (0.5 microM) or to an excess of K+ (28 and 56 mM instead of 5.6 mM). The K+-evoked release was totally dependent on the presence of Ca2+ in the superfusing fluid whereas the spontaneous efflux of MELM was only partially Ca2+-dependent. Further experiments performed with tissues of polyarthritic rats indicated that the increase in their MELM levels was associated with a lower fractional rate constant of MELM release, therefore suggesting that spinal Met-enkephalin turnover might be reduced in chronically suffering animals. Examination of the possible modulation of MELM release by various neuroactive compounds present within the dorsal horn revealed that cholecystokinin (10 microM), but not its desulphated derivative, substance P-sulphoxide (10 microM), and to a lesser extent substance P, enhanced the K+-evoked MELM release. In contrast, gamma-aminobutyric acid (10 microM) and (-)-baclofen (1 microM) partially prevented the stimulatory effect of K+ on MELM release. Other compounds such as serotonin, somatostatin, and neurotensin altered neither the spontaneous nor the K+-evoked release of MELM.
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PMID:Basic and regulatory mechanisms of in vitro release of Met-enkephalin from the dorsal zone of the rat spinal cord. 674 33


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