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)

The present study examines the effects of intrathecal administration of selected peptides on nociceptive responses in the rat. Each peptide was delivered via a chronically implanted catheter to the L5 vertebral level. In the tail flick test, VIP (0.65-6.5 nmoles) produced a dose-dependent decrease in reaction time (RT) from 1 to 6-16 min after injection; 6.5 nmoles decreased RT to 37% of control value at 1 min after injection. Galanin (0.65-6.5 nmoles) produced a dose-dependent increase in reaction time at 1 and 6 min; at high doses, many of the rats failed to flick the tail. CGRP (6.5 nmoles) produced a small, transient decrease in RT to 73% of control values at 1 min; 3.25 nmoles were without effect. CSF and 6.5 nmoles of somatostatin, TRH and angiotensin II were without effect. At high doses of galanin and CGRP, rats vocalized to innocuous touch of the tail, as reported for substance P. Von Frey hairs were thus applied to the tail after 6.5 nmoles of VIP, galanin, CGRP or substance P. Vocalization in response to a previously innocuous pressure stimulus was observed at 30 s after injection in all rats given galanin and some rats given CGRP or substance P; the effect lasted 4-8 min. VIP and CSF had no effect. These results suggest that VIP, galanin, CGRP and substance P may act as excitatory agents in nociceptive pathways and that specific peptides may function in the different types of pain modalities; VIP in thermal, galanin in mechanical and substance P and CGRP in both.
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PMID:Effects of intrathecal administration of neuropeptides on a spinal nociceptive reflex in the rat: VIP, galanin, CGRP, TRH, somatostatin and angiotensin II. 245 92

Galanin has been shown to be present in the gastrointestinal tract, pancreas and CNS. In the rat stomach, immunohistochemical studies have revealed the presence of galanin in the intrinsic nervous system suggesting a function as putative neurotransmitter or neuromodulator which could affect neighbouring exo- or endocrine cells. Therefore this study was performed to determine the effect of galanin on the secretion of gastrin and somatostatin-like immunoreactivity (SLI) from the isolated perfused rat stomach. The stomach was perfused via the celiac artery and the venous effluent was collected from the portal vein. The luminal content was kept at pH 2 or 7 Galanin at a concentration of 10(-10), 10(-9) and 10(-8) M inhibited basal gastrin release by 60-70% (60-100 pg/min; p less than 0.05) at luminal pH 7. At luminal pH 2 higher concentrations of galanin (10(-9) and 10(-8) M) decreased basal gastrin secretion by 60-70% (60-100 pg/min; p less than 0.05). This inhibitory effect was also present during infusion of neuromedin-C, a mammalian bombesin-like peptide that stimulates gastrin release. SLI secretion remained unchanged during galanin administration. The inhibitory action of galanin on gastrin secretion was also present during the infusion of tetrodotoxin suggesting that this effect is not mediated via neural pathways. The present data demonstrate that galanin is an inhibitor of basal and stimulated gastrin secretion and has to be considered as an inhibitory neurotransmitter which could participate in the regulation of gastric G-cell function.
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PMID:Effect of galanin on gastrin and somatostatin release from the rat stomach. 245 73

Calbindin D28k, previously demonstrated in the mammalian central nervous system, has been localized to discrete neurons in the enteric nervous system of the rat. Calbindin D28k is present in cell bodies in both the myenteric and submucous plexi and in interganglionic nerve fibers in all regions of the gastrointestinal tract. Immunoreactive nerve fibers were also detected in the mucosal region, although none were observed in the pyloric sphincter, circular or longitudinal muscle layers. The highest concentration of immunoreactivity was present in the submucosal plexus and mucosa of the colon. Western blot analysis of the protein detected by the antiserum confirmed that it comigrated with purified calbindin D28k and the single immunoreactive band seen in extracts from rat brain. The colocalization of calbindin D28k with components of the peptidergic innervation was also investigated. Of the peptides studied the neurons containing both vasoactive intestinal polypeptide and neuropeptide Y in the submucous plexus were seen to exhibit calbindin D28k immunoreactivity. The neurons containing somatostatin, galanin and substance P did not demonstrate co-localization. In the stomach, calbindin D28k was detected within a small number of epithelial cells which were found to correspond to a sub-population of the somatostatin-immunoreactive endocrine cells.
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PMID:Distribution and co-localization of calbindin D28k with VIP and neuropeptide Y but not somatostatin, galanin and substance P in the enteric nervous system of the rat. 245 56

In four conscious dogs infusions of glucose (1 g/kg/h) alone or glucose and galanin (2 micrograms/kg/h) were undertaken during cryogenic vagal blockade at -2 degrees C or following atropine (100 micrograms/kg i.v.). When compared to parenteral glucose alone, the addition of galanin substantially elevated plasma glucose and blunted plasma insulin responses. Vagal blockade or atropine failed to alter these effects of galanin on plasma insulin or glucose responses. Moreover, plasma levels of somatostatin, pancreatic glucagon, pancreatic polypeptide, growth hormone, and cortisol were unaffected by galanin infusions. Thus, the inhibition of plasma insulin responses to glucose by galanin is mediated by a nonvagal, noncholinergic mechanism and is independent of changes in either plasma pancreatic glucagon or somatostatin levels. Galanin at the dose employed in the study may have direct and selective actions on the B cell and thus play an important role in the neuromodulation of insulin release.
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PMID:Effect of galanin and vagal integrity on insulin release in dogs. 245 71

Exogenous galanin has been shown to suppress insulin secretion as elicited by a number of secretagogues such as glucose, arginine, tolbutamide, carbachol, and oral nutrients. To achieve further insight into the influence of galanin on the endocrine pancreas, we have investigated the effect of synthetic porcine galanin (a 200 ng bolus followed by constant infusion at a concentration of 16.8 ng/mL for 16 to 24 minutes) on unstimulated insulin, glucagon, and somatostatin release, as well as on the responses of these hormones to 1 nmol/L vasoactive intestinal peptide (VIP), 1 nmol/L gastric inhibitory peptide (GIP), 1 nmol/L 26 to 33 octapeptide form of cholecystokinin (8-CCK) or 10 nmol/L glucagon in the perfused rat pancreas. Galanin infusion reduced unstimulated insulin secretion by 60% without modifying glucagon and somatostatin output. Galanin also blocked insulin release elicited by VIP, GIP, and 8-CCK, it did not affect the glucagon responses to VIP and GIP, or the somatostatin responses to VIP, GIP, and 8-CCK. Finally, galanin inhibited the insulin output, but not the somatostatin release induced by glucagon. In conclusion, in the perfused rat pancreas, galanin appears to behave as a general inhibitor of insulin secretion. Since this neuropeptide does not modify glucagon or somatostatin release, a direct effect of galanin on the B-cell seems plausible.
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PMID:Effects of galanin on islet cell secretory responses to VIP, GIP, 8-CCK, and glucagon by the perfused rat pancreas. 245 42

The effects of sympathetic neural activation on basal pancreatic hormone secretion cannot be explained solely by the actions of the classic sympathetic neurotransmitter norepinephrine. The nonadrenergic component may be mediated by the 29-amino acid peptide galanin in that this neuropeptide meets several of the criteria necessary to be considered a sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin administration inhibits basal insulin and somatostatin secretion and stimulates basal glucagon secretion from the pancreas, qualitatively reproducing the effects of sympathetic nerve stimulation. These sympathomimetic effects appear to be mediated by direct actions of galanin on the islet. 2) Galanin-like immunoreactivity exists in fibers that innervate pancreatic islets. 3) Galanin is released during electrical stimulation of pancreatic nerves. The quantity released is sufficient to reproduce sympathetic nerve stimulation-induced effects on insulin secretion and to contribute to the neural effects on somatostatin and glucagon release. 4) Whether interference with galanin action or release reduces the islet response to sympathetic nerve stimulation remains to be determined. We hypothesize that galanin and norepinephrine act together to mediate the islet response to sympathetic neural activation. If galanin is a sympathetic neurotransmitter in the endocrine pancreas, it may contribute to the inhibition of insulin secretion that occurs during stress and thereby to the hyperglycemic response. Moreover, the local presence of this potent beta-cell inhibitor in the islet leads to speculation on galanin's contribution to the impairment of insulin secretion that occurs in non-insulin-dependent diabetes mellitus and therefore on the potential utility of a galanin antagonist in the treatment of this disease.
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PMID:Galanin--sympathetic neurotransmitter in endocrine pancreas? 245 28

The immunohistochemical occurrence of several different neuronal markers has been investigated in human gingiva with phenytoin-induced overgrowth. The material was compared to gingival material taken following surgical orthodontic treatment. Gingiva obtained from the phenytoin-treated groups seemed to have a reduced number of neurofilament (NF) immunoreactive nerve fibers in the propria compared to control material. In both phenytoin as well as control gingiva sparsely distributed, thin, calcitonin gene-related peptide (CGRP) and substance P (SP) immunoreactive fibers were found in the propria. No obvious differences between the two groups could be observed for CGRP and SP. Immunoreactive cells for somatostatin (SOM) with a dendritic cell shape were found in the propria in both groups, sometimes in densely packed clusters. A tendency for increase of SOM-immunoreactive cells in the phenytoin-treated gingiva was observed. A few gamma-melanocyte stimulating hormone (gamma-MSH)-immunoreactive cells with a round appearance were found in control as well as phenytoin-affected gingiva. In one instance, however, a heavy gamma-MSH-immunoreactive cell infiltration was seen in the phenytoin sample. No immunoreactivity in either the phenytoin-treated group or in the control group was seen for proctolin or galanin. The results indicated that gingiva with phenytoin-induced overgrowth has a reduced innervation density revealed with NF immunohistochemistry.
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PMID:Immunohistochemical study of neuronal markers in human gingiva with phenytoin-induced overgrowth. 245 33

Galanin is a 29 amino acid peptide which has been found in intrapancreatic nerves. The effects of galanin, adrenergic and cholinergic blockade as well as somatostatin on the hormone release from the isolated perfused dog pancreas were studied. It was found that galanin dose-dependently inhibited insulin (P less than 0.001) and somatostatin (P less than 0.001) but not glucagon secretion at normal glucose levels. The lowest galanin concentration that caused a significant suppression of insulin and somatostatin secretion was 10(-11) and 10(-10) mol/l, respectively. Similar effects were evident during stimulation with 2.5 mmol/l arginine. Galanin (10(-9) mol/l) caused a more pronounced inhibition of insulin and somatostatin secretion at high (10 mmol/l) and normal (5 mmol/l) than at low glucose (1.3 mmol/l). In contrast, suppression of the glucagon secretion was only seen at low glucose (1.3 mmol/l). Perfusion of 10(-6) mol/l of atropine, phentolamine and propranolol had no effect on the galanin-mediated (10(-10) mol/l) inhibition of insulin and somatostatin secretion. Galanin (10(-12)-10(-10) mol/l) and somatostatin (10(-12)-10(-10) mol/l) were equipotent in inhibiting insulin secretion whereas only somatostatin exerted a suppression of the glucagon secretion at normal glucose. Thus, galanin exerts a differential effect on islet hormone secretion and may participate in the hormonal control of insulin, glucagon and somatostatin secretion.
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PMID:Effects of galanin on the release of insulin, glucagon and somatostatin from the isolated, perfused dog pancreas. 245 6

Punch biopsies were obtained from the buccal gingiva of the lower third molars. Thin nerve fibres, immunoreactive for calcitonin gene-related peptide (CGRP) or substance P (SP), with possible sensory function, were found in the propria often close to the epithelium, sometimes even penetrating into the basal layers. gamma-Melanocyte stimulating hormone (gamma-MSH)-like immunoreactivity was found in sparsely distributed single cells (except in one specimen containing a dense infiltration), resembling neutrophilic granulocytes of the propria. gamma-MSH was present in several single smooth axons and in thick axon bundles of the propria. Surrounding the blood vessels, neuropeptide Y (NPY), tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine amide (PHI) immunoreactive nerve fibres were observed. NPY and TH-positive fibres probably represent sympathetic nerve terminals and VIP/PHI-immunoreactive ones may have a parasympathetic function. Papillae of the propria contained VIP-positive fibres not obviously related to blood vessels. The distribution in papillae of PHI-like immunoreactivity was similar but the PHI-positive reaction was also present in a few cells of the propria, especially near blood vessels. Somatostatin (SOM)-positive reaction occurred in a few dendritic-type cells near or in the epithelium and single nerve fibres close to the epithelium. Several thick axon bundles of the propria contained neurofilament (NF)-immunoreactive material. Some thin NF-fibres were found in the papillae and some seemed to penetrate into the epithelium. No galanin, methionine-enkephalin, parathyroid hormone or proctolin immunoreactive material was found. The rather rich content of several neuropeptides in human attached gingiva, as well as other neurochemical markers, is probably associated with sensory and autonomic functions.
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PMID:Immunohistochemical studies of the neurochemical markers, CGRP, enkephalin, galanin, gamma-MSH, NPY, PHI, proctolin, PTH, somatostatin, SP, VIP, tyrosine hydroxylase and neurofilament in nerves and cells of the human attached gingiva. 246 71

The effect of cholinergic blockade with pirenzepine or atropine on growth hormone (GH) release after galanin administration was investigated in five normal male subjects. The mean peak GH response to an infusion of galanin (40 pmol/kg/min for 40 minutes) was significantly reduced from 17.2 mU/L to 2.9 mU/L (P less than .001) with prior administration of pirenzepine (30 mg IV). When galanin was infused at a higher dose (80 pmol/kg/min), this suppression of release by pirenzepine was partially overcome, with GH rising to a mean peak response of 8.0 mU/L (P less than .05). Repeated administration of atropine (two bolus doses of 0.6 mg IV) also failed to abolish the GH response to this higher dose of galanin in two subjects. It has been proposed that cholinergic pathways control GH release via somatostatin, and this study suggests that galanin may also act by modulating hypothalamic somatostatinergic tone either directly or by facilitating cholinergic transmission.
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PMID:The effect of cholinergic blockade on the growth hormone response to galanin in humans. 246 Jul 22


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