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)

EEG sleep recordings were performed in rats under intraperitoneal injections of saline, desipramine (DMI, 4 mg/kg) an inhibitor of noradrenaline reuptake, and DMI plus the octapeptide somatostatin analogue (octreotide, 0.2 mg/kg). As already reported, DMI resulted in selective suppression of paradoxical sleep (PS) and increased slow wave sleep (SWS). The administration of the octapeptide somatostatin analogue totally reversed the DMI-induced suppression of PS, but had no effect on SWS. This finding confirms previous results demonstrating a role of somatostatin in the generation of PS. In addition, it suggests that the suppression of PS by DMI may be due to an inhibitory effect on somatostatin release, rather than to an alteration of brain noradrenaline.
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PMID:Reversal of desipramine-induced suppression of paradoxical sleep by a long-acting somatostatin analogue (octreotide) in rats. 256 65

This study investigated the in vivo neuronal release of somatostatin in the rat nucleus accumbens (NAc), and the effect of chronic administration of antidepressants. Microdialysis studies were performed on male Sprague-Dawley rats, in accordance with the EU guidelines (EEC Council 86/609). Somatostatin levels were quantified by radioimmunoassay (RIA) or enzyme linked immuno sorbent assay (ELISA). A high concentration of potassium ions (K(+), 100 mM) was used to ascertain the neuronal release of somatostatin. Antidepressant treatments involved the administration of citalopram (20 mg/2 ml/kg, i.p., once daily) or desipramine (DMI, 5 mg/2 ml/kg, i.p., twice daily) for 21 days. Control groups received saline (2 ml/kg for 21 days, i.p.) once or twice daily respective of the antidepressant treatment. Basal levels of somatostatin released were found to be 20.01+/-0.52 fmol/sample. K(+) (100 mM) increased somatostatin levels at 205% of basal. Chronic citalopram and desipramine treatments also increased the somatostatin levels by 83+/-32% and 40+/-6% of basal, respectively. These findings indicate that somatostatin is released neuronally in the NAc. Antidepressants influence its release in a positive manner, suggesting the necessity of further studies for the elucidation of the involvement of somatostatin in the putative therapeutic effects of these agents.
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PMID:Chronic antidepressant treatment modulates the release of somatostatin in the rat nucleus accumbens. 1629 66