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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 .