The effects of scheduled running wheel access on binge-like eating behavior and its consequences.

Binge eating disorder (BED) is an eating disorder involving repeated, intermittent over consumption of food in brief periods of time, usually with no compensatory behaviors. There are few successful treatments and the underlying neural mechanisms remain unclear. In the current study, we hypothesized that voluntary running wheel (RW) activity could reduce binge-like eating behavior in a rat model.

Failure to upregulate Agrp and Orexin in response to activity based anorexia in weight loss vulnerable rats characterized by passive stress coping and prenatal stress experience.

We hypothesize that anorexia nervosa (AN) poses a physiological stress. Therefore, the way an individual copes with stress may affect AN vulnerability. Since prenatal stress (PNS) exposure alters stress responsivity in offspring this may increase their risk of developing AN.

Neuroprotective effects of PPAR-γ agonist rosiglitazone in N171-82Q mouse model of Huntington's disease.

Huntington's disease (HD) is a devastating genetic neurodegenerative disease caused by CAG trinucleotide expansion in the exon-1 region of the huntingtin gene. Currently, no cure is available. It is becoming increasingly apparent that mutant Huntingtin (HTT) impairs metabolic homeostasis and causes transcriptional dysregulation.

Stress vulnerability during adolescent development in rats.

Adolescent development is proposed to represent a time of increased susceptibility to stress. During adolescence, the brain demonstrates a high level of plasticity and can be positively or negatively affected by the environment. This study tests the hypothesis that adolescent development is a stage of enhanced vulnerability to chronic stress.

Stress activation of IL-6 neurons in the hypothalamus.

An emerging literature attests to the ability of psychological stress to alter the inflammatory cytokine environment of the body. While the ability of stress to cause cytokine release is well established, the neural pathways involved in this control have yet to be identified. This study tests the hypothesis that IL-6 neurons of the hypothalamo-neurohypophyseal system (HNS), a neural pathway proposed to secrete IL-6 into the circulation, are activated in response to psychological stress.