Decreased excitability of leptin-sensitive anterior insula pyramidal neurons in a rat model of compulsive food demand.

Compulsive eating is an overlapping construct with binge eating that shares many characteristics with substance use disorders. Compulsive eating may impact millions of Americans; presenting in some cases of binge eating disorders, overweight/obesity, and among individuals who have not yet been diagnosed with a recognized eating disorder. To study the behavioral and neurobiological underpinnings of compulsive eating, we employ a published rodent model using cyclic intermittent access to a palatable diet to develop a self-imposed binge-withdrawal cycle.

Intermittent, extended access to preferred food leads to escalated food reinforcement and cyclic whole-body metabolism in rats: Sex differences and individual vulnerability.

Compulsive binge eating is a hallmark of binge eating disorder and bulimia nervosa and is implicated in some obesity cases. Eating disorders are sexually dimorphic, with females more often affected than males. Animal models of binge-like eating based on intermittent access to palatable food exist; but, little is known regarding sex differences or individual vulnerability in these models with respect to the reinforcing efficacy of food, the development of compulsive- and binge-like eating, or associated changes in whole-body metabolism or body composition.

Nuclear receptor coactivators function in estrogen receptor- and progestin receptor-dependent aspects of sexual behavior in female rats.

The ovarian hormones, estradiol (E) and progesterone (P) facilitate the expression of sexual behavior in female rats. E and P mediate many of these behavioral effects by binding to their respective intracellular receptors in specific brain regions. Nuclear receptor coactivators, including Steroid Receptor Coactivator-1 (SRC-1) and CREB Binding Protein (CBP), dramatically enhance ligand-dependent steroid receptor transcriptional activity in vitro.