l796778 and Encephalitis

Glial inflammation plays an integral role in the development of neurodegenerative disease. Although somatostatin is known to be a local anti-inflammatory factor in the periphery, evidence of a similar function in the brain is scarce. The aim of the present study was to investigate the effect of somatostatin on prostaglandin E(2) synthesis in primary neonatal rat glial cells. The data shows that high concentrations of somatostatin (10(-5)-10(-4)) significantly increased prostaglandin synthesis. By contrast, when used at physiologically relevant concentrations (10(-9)-10(-7) M), somatostatin and somatostatin receptor agonists decreased prostaglandin E(2) synthesis in non-stimulated glial cells as well as in lipopolysaccharide-induced prostaglandin synthesis. The inhibitory effect of somatostatin in lipopolysaccharide-treated cells could be mimicked by protein kinase A inhibitor and was prevented by forskolin. These observations suggest the presence of a novel neuro-immune feedback pathway through which somatostatin inhibits glial prostaglandin synthesis, and thus may prove to play a role in brain inflammation. This action of somatostatin may have a therapeutic potential in pathological conditions of the brain, where an inflammatory response is involved.

Topics: Amides; Animals; Animals, Newborn; Brain; Cells, Cultured; Colforsin; Culture Media; Culture Media, Serum-Free; Dinoprostone; Dose-Response Relationship, Drug; Encephalitis; Hormone Antagonists; Indoles; Isoquinolines; Lipopolysaccharides; Neuroglia; Nitrobenzenes; Octreotide; Radioimmunoassay; Rats; Rats, Wistar; Receptors, Somatostatin; Somatostatin; Sulfonamides