Two classes of neuropeptides, somatostatin and the endogenous opioids, have been highly conserved during evolution, are expressed in early stages of embryogenesis, and function through similar families of G-protein coupled receptors. To investigate their roles in development and in adult function, we are systematically mutating the genes for somatostatin and its five receptors, and for the three endogenous opioid encoding genes. We have introduced a null allele at the somatostatin and at the proopiomelanocortin locus in the mouse germline. We have analyzed the mutant mice lacking somatostatin in detail. Initially following hypotheses about the function of somatostatin derived from literature data, we did not find significant changes in endocrinological parameters (growth hormone, thyroid stimulating hormone, insulin). However, when applying a non-hypothesis-driven, systematic scan for a phenotype, we identified novel interesting aspects of somatostatin function.
