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

Immunoreactive-somatostatin (IR-SRIF) levels were investigated in the brain of 4 types of ataxic mice (Rolling Mouse Nagoya, Weaver, PCD, Staggerer) with different cerebellar pathologies. IR-SRIF concentrations (ng/mg) were found to be significantly elevated in both cerebellum and cerebrum of all ataxic mutant mice, IR-SRIF (ng/organ) was found to be increased in the cerebellum and cerebrum in Rolling Mouse Nagoya and PCD compared with control mice. The gel-filtration profile (Sephadex G-50) in the cerebellar extracts of Rolling Mouse Nagoya proved to be identical to that of control mice. Three peaks of IR-SRIF were found to be uniformly elevated in Rolling Mouse Nagoya, with the highest peak coinciding with authentic somatostatin-14. The present results suggest that elevated levels of IR-SRIF in the brain may play a role in the mechanism underlying the manifestation of ataxia in ataxic mutant mice, especially in Rolling Mouse Nagoya and PCD.
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PMID:[Elevated immunoreactive-somatostatin levels in the brain of ataxic mutant mice]. 290 64

The role of serotonin (5-HT) in the regulation of growth hormone (GH) secretion remains unclear due to the existence of many different receptors that mediate the 5-HT actions, and the lack of suitable specific agonist and antagonist drugs. In the present work we have taken advantage of the recent development of new selective 5-HT drugs in order to clarify the role played by different 5-HT receptor types and subtypes on GH secretion. The experiments were carried out on beagle dogs. GH-releasing hormone (GHRH) increased basal canine GH (cGH) levels from 0.8 +/- 0.2 to 8.8 +/- 1.7 microg/l at 15 min. Administration of 5-HT(1D) receptor agonist sumatriptan (SUM) induced a cGH peak at 30 min of 12.9 +/- 2.7 microg/l. The combined administration of GHRH plus SUM strikingly potentiated cGH release with a peak of 36.9 +/- 6 microg/l at 30 min (p < 0.05). Pretreatment with the muscarinic receptor antagonist atropine completely abolished the cGH response to SUM, while the cholinergic agonist pyridostigmine (PYR) did not modify this response (15.3 +/- 5 microg/l PYR plus SUM vs. SUM alone 12.9 +/- 2. 7 microg/l). On the other hand, administration of drugs with activity at 5-HT(2A/C) receptors showed a stimulatory role for the 5-HT(2C) receptor subtype, since LY-53857 (antagonist 5-HT(2A/C)) and DOI agonist (5-HT(2A/C)) both modified the GH response stimulated by GHRH (AUC 88.5 +/- 30.4 and 400 +/- 64.6 vs. 267.3 +/- 52.6 respectively), while ketanserin (antagonist 5-HT(2A)) did not modify this response. The 5-HT(3) antagonist ICS-205-930 failed to modify either basal or GHRH induced GH responses. In conclusion, our data show that 5-HT(1D) receptors play a stimulatory role on GH secretion in the dog, possibly by acting through a decrease in hypothalamic somatostatin release. Similarly, the 5-HT(2C) receptor subtypes also appear to play a stimulatory role. However, 5-HT(2A) and 5-HT(3) receptors do not appear to be involved in the control of basal and GHRH-induced GH secretion.
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PMID:Influence of different serotonin receptor subtypes on growth hormone secretion. 1068 28