PMC:4195273 / 94418-96087 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4195273","sourcedb":"PMC","sourceid":"4195273","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4195273","text":"Overexpression of central CART through i.c.v. injections at either the forebrain (LV), interbrain (3V) or hindbrain (4V) areas has conformed to an anorexigenic role of CART, while the appetite-promoting effects of CART administered into specific neuronal targets may be attributed to a role of hypothalamic CART in stimulating the local release of orexigenic neuropeptides in a hypothalamic nucleus-specific manner. The discrepancy in anorexigenic and orexigenic circuitry highlights the major pitfall of non-specific widespread effects associated with i.c.v. ligand delivery, and was recognized through the efforts to identify potential sites for CART action following the analysis of Fos expression pattern representative of i.c.v. CART-induced neuronal activities. Candidate sites that may house the key mediator for the hypophagic effects of i.c.v. CART primarily reside in various feeding-related areas, including major hypothalamic nuclei, specific brainstem structures, and the Acb of the cerebral striatum. The appetite-inhibiting and -promoting effects produced by intra-accumbal CART and CART siRNA respectively reflect a concerted response from the CART-dopaminergic system interaction within the Acb, hence the observed feeding modulation and locomotive effects were likely perplexed by the inherent reward and motivation pathway. Several hindbrain areas are of particular interest as alternative brain regions for CART-induced anorexic effects, owing to the well-described role of the hindbrain in conveying post-prandial satiety effects to the hypothalamus, consonant with the indicated relation between CART and vagally-mediated gastrointestinal satiety.","tracks":[]}