Ghrelin signaling is required for escalation in high-fat intake during repeated binge eating episodes

VALDIVIA S; CORNEJO M P; DE FRANCESCO P N; GARCÍA ROMERO G; REYNALDO M; PERELLÓ M

Huerta Grande, Córdoba

Congreso; XXIX CONGRESO ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACION EN NEUROCIENCIAS; 2014

Sociedad Argentina de Investigación en Neurociencias

Many people suffering eating disorders display binge eating episodes, in which an excessive amount of palatable foods is rapidly consumed. Ghrelin is a stomach derived hormone that strongly increases food intake. Little is known about the neuronal circuitries activated during binge eating episodes or the role of ghrelin on this behavior. Here, we used a combination of behavioral and neuroanatomical studies in genetically or pharmacologically manipulated mice to determine the neuronal brain centers activated in a binge eating model induced by intermittent access to high fat diet (HFD). We also examined the potential role of ghrelin in the modulation of this behavior. First, we confirmed that Intermittent and limited access to HFD induces binge eating events with an escalating profile. By using c-Fos immunostaining, we found that HFD binging activated neuronal populations of the mesolimbic pathway, including dopamine-neurons of the ventral tegmental area (VTA) and orexin neurons of the lateral hypothalamus. Orexin signaling blockage failed to affect escalation of HFD binging events and c-Fos induction in the VTA. Interestingly, ghrelin signaling was required for escalation of HFD binging events and full c-Fos induction in the VTA. Thus, we conclude that ghrelin signaling is required for escalation in HFD intake during repeated binge eating episodes presumably by regulating the sensitivity of the mesolimbic pathway to the rewarding stimulus.