Cellular Mechanisms and Neural Control of Sodium Appetite in Male Rats

摘要: Sodium appetite is a reliable and robust behavior displayed by broad range of species. Despite its key role in survival, the biological basis this remains undefined. The goal thesis to elucidate cellular signaling neural circuitry underlying sodium appetite. More specifically, I focus on central actions hormones aldosterone Angiotensin II (AngII) eliciting crucial ingestive behavior. First, tested hypothesis that protein downstream AngII receptor, Mitogen Activated Protein Kinase (MAPK), underlies induced endogenous AngII. demonstrated through both behavioral pharmacology expression requires MAPK activation but thirst does not. Next, potentiate inactivation an inhibitory signal. Using functional neuroanatomy reversible lesions, revealed cooperativity between involves alleviation oxytocin signal relayed from paraventricular nucleus hypothalamus organum vasculosum lateral terminalis. Finally, increase motivation for associated with mesolimbic dopamine activity. progressive ratio schedule reinforcement neuroanatomy, discovered combination induces selective drive sodium, which activity markers synthesis ventral tegmental area accumbens. Together, these findings demonstrate important AngII-induced appetite, potentiation plus inhibition secretion circuitry.