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Brain Somatostatin Receptors Are Up-Regulated In Somatostatin-Deficient Mice

Fraser Laboratories (J.L.R., R.M., U.K., Y.C.P.), Departments of Medicine, Pharmacology and Therapeutics, Neurology and Neurosurgery, McGill University and Royal Victoria Hospital, Montréal, Québec, Canada, H3A 1A1; and The Vollum Institute (V.O.C., M.R., M.J.L.), Oregon Health & Science University, Portland, Oregon 97201

Address all correspondence and requests for reprints to: Dr. Y. C. Patel, Room M3-15, Royal Victoria Hospital, 687 Pine Avenue West, Montréal, Québec H3A 1A1, Canada. E-mail: yogesh.patel{at}mcgill.ca.

The peptide somatostatin (SST) is widely synthesized in the brain and periphery and acts through a family of five receptors (SSTR1-5) to exert numerous effects. A gene product related to SST, cortistatin (CST), also interacts with SSTR1-5. Here we have investigated the regulation of SSTR1-5 and of CST in SST knockout (SSTKO) mice. The five SSTRs were quantitated individually by subtype-selective binding analysis, by immunocytochemistry, and by mRNA measurement and showed, in the brain of SSTKO mice, up-regulation of subtypes 1, 2, 4, and 5, and down-regulation of SSTR3. Peripheral tissues displayed both subtype- and tissue-specific changes in SSTR1-5 mRNA levels of expression. Lack of SST did not up-regulate normal CST expression in brain nor did it induce its expression in the periphery. SST-like immunoreactivity, however, was induced in the proximal midgut in SSTKO animals, suggesting intestinal expression of a novel SST-like gene.

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