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 effects of somatostatin (SOM) and cholecystokinin octapeptide (CCK-8) on basal and potassium-induced release of acetylcholine (ACh) were investigated in slices of rat caudate nucleus (CN) and, for comparison, cerebral cortex (CX). Potassium (5-55 mM) produced a concentration-dependent increase in the release of [3H]ACh in the presence of extracellular Ca2+. SOM (1 microM), CCK-8 (1 microM) and the dopamine (DA) receptor agonist, apomorphine (APO, 30 microM) inhibited the K+-induced (35 mM) release of [3H]ACh by 26-32% from CN, but did not affect ACh release from CX. Other peptides (1 microM), such as Met-enkephalin, vasoactive intestinal peptide, thyrotropin-releasing hormone and substance P, had no effect on release of [3H]ACh in CN or CX. Sulpiride (SULP), a dopamine receptor antagonist, prevented the effects of APO and SOM, but not CCK-8, to inhibit [3H]ACh release. The results indicate that: (1) SOM and CCK-8 inhibit the release of [3H]ACh in CN, but not CX; and (2) the inhibitory effect of SOM, but not CCK-8, on [3H]ACh release is mediated by dopaminergic mechanisms.
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PMID:Somatostatin and cholecystokinin octapeptide differentially modulate the release of [3H]acetylcholine from caudate nucleus but not cerebral cortex: role of dopamine receptor activation. 287 39

The present study investigates the effects of the administration of an intracerebroventricular (i.c.v.) dose of 500 micrograms/rat of the neuroleptic (-) sulpiride on somatostatin-like immunoreactivity (SSLI) levels, 125I-Tyr11-SS binding to its specific receptors, SS-modulated adenylyl cyclase (AC) activity and the pertussis toxin (PTX) substrates measured by toxin-catalysed ADP ribosylation of the alpha-subunits from G-proteins. (-) Sulpiride significantly decreased the SSLI levels in the frontoparietal cortex at 30 min but was without effect on the SSLI concentration in the striatum. This decrease had disappeared within 24 hr. The administration of (-) sulpiride produced a significant increase in the number of 125I-Tyr11-SS receptors and a significant reduction in their affinity at 30 min after injection in the striatum without affecting the frontoparietal cortex. The effects of the (-) sulpiride injection had disappeared after 24 hr. This change in SS binding was not due to a direct effect of (-) sulpiride on these receptors since no effect on binding was produced by high concentrations of (-) sulpiride (10(-5) M) when added in vitro. No significant differences were seen in either brain region for the basal or the forskolin (FK)-stimulated AC enzyme activities in the control and (-) sulpiride groups. In the (-) sulpiride group, the capacity of SS to inhibit FK-stimulated AC in the frontoparietal cortex was significantly higher than in the control group with no significant difference in the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of sulpiride on somatostatin receptors, somatostatin-like immunoreactivity and modulation of adenylyl cyclase activity in the rat brain. 793 12

Reduced levels of somatostatin and neuropeptide Y (NPY) have been demonstrated in the brain of patients with some organic mental disorders. We designed the present study to test whether drugs thought to be effective in improving cognitive functions in these disorders increased the levels of these two peptides. The drugs were given to normal rats for 14 days to examine chronic effects on regional brain somatostatin and NPY levels. Amantadine and bifemelane increased these peptide levels. Idebenone and indeloxazine had little effect. The effect of dopaminergic agents on peptide levels was also tested in rats. 1-Dihydroxyphenylalanine increased somatostatin levels in whole brain, and hypothalamic NPY levels, and reduced NPY levels in the cerebral cortex, hippocampus and striatum. Sulpiride increased the levels of NPY in the striatum and brainstem. 6-Hydroxydopamine decreased cortical somatostatin levels, and increased striatal NPY levels. These findings indicate that some agents used to improve cognitive function impairment in organic mental disorders may increase somatostatin and NPY content in the brain of rats. Also, it is suggest that these peptides are under different influences of the dopaminergic system in the brain.
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PMID:Effects of putative cognitive function-enhancing drugs and dopaminergic agents on somatostatin and neuropeptide Y in rat brain. 809 19