title: Brain gastrin/CCK immunoreactivity in sand rat (Psammomys obesus): decrease of number of positive neurons in diabetic animals.
abstract: Gastrin/CCK immunoreactivity appears to be widely distributed throughout the mammalian CNS, being most abundant in the cerebral cortex [Vanderhaeghen et al. 1975; Straus et al. 1977; Beinfeld et al. 1981]. Besides its putative role as a co-transmitter in dopaminergic neurotransmission [Hökfelt et al. 1980], cholecystokinin is apparently involved in the central regulation of appetite and satiety [Gibbs et al. 1973; Antin et al. 1975; Parret and Batt 1980; Smith 1980; Smith and Gibbs 1981] Furthermore, it has been shown that the brain concentration of the peptide is decreased in genetically obese mice as compared to non-obese animals [Strauss and Yalow 1979]. The sand rat (Psammomys obesus) is a desert rodent which tends to become diabetic when it is fed with normocaloric diet and restricted in movement [Haines et al. 1965; Hahn et al. 1971]. However, the usefulness of this animal as a paradigm of diabetes is now being revised, since because in its typical expression this metabolic dysfunction appears to be an obesity syndrome [Rice and Robertson 1980]. Therefore, it seems to be necessary to study the distribution of gastrin/CCK-immunoreactive nerve cells in the brain of normal and diabetic (obese) sand rats to get further information about mechanism underlying the development of this form of diabetes.
mesh_terms: D000818:Animals; D003411:Arvicolinae; D002452:Cell Count; D002540:Cerebral Cortex / Q000032:analysis* / Q000473:pathology; D002766:Cholecystokinin / Q000032:analysis*; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000473:pathology; D005755:Gastrins / Q000032:analysis*; D007124:Immunoenzyme Techniques; D009474:Neurons / Q000032:analysis* / Q000473:pathology; D009765:Obesity; D011817:Rabbits
chemical_list: D005755:Gastrins; D002766:Cholecystokinin