Neuronal populations involved in binge eating behaviors

SPRING VALDIVIA; AGUSTINA CABRAL; ANABELA PATRONE; GIMENA FERNÁNDEZ; MIRTA REYNALDO; MARIO PERELLO

Congreso; XXVII congreso de la SAN; 2012

Binge eating is defined as repeated, discrete and intermittent bouts of consuming unusually large amounts of food. This eating disorder affects 6% of the general population and it is associated to diverse body weight-related pathologies from obesity to anorexia nervosa. The neuronal circuitries and neurotransmitters involved in this behavior are currently unclear. Here, we developed a model of high fat diet (HFD) bingeing in mice and characterized theneuronal systems activated. Using double immunostaining for tyrosine hydroxylase, as a marker of dopaminergic neurons, and c-fos, as a marker of neuronal activation, we found that HFD bingeing activates the meso-limbic pathway. In particular, binge eating recruits dopaminergic neurons of the paranigral and interfascicular subdivisions of the ventral tegmental area. Using a transgenic mouse model that expresses green fluorescent protein in the corticotrophin-releasing factor (CRF)-producing neurons, we found that CRF neurons of the central amygdala are also recruited by HFD bingeing. In contrast, the nucleus accumbens of the ventral striatum failed to show signs of activation in our experimental paradigm. Thus, we conclude that HFD bingeing activates specific dopaminergic and CRF neurons of the reward-related central circuitries.