OASIS

Presentation Abstract

Program#/Poster#:	187.27/TT6
Title:	Long-term alterations in behavior and stress and reward pathways following high fat diet withdrawal
Location:	Hall A-C
Presentation Time:	Sunday, Nov 16, 2008, 10:00 AM -11:00 AM
Authors:	*S. L. TEEGARDEN, T. L. BALE; Dept Animal Biol, Univ. Pennsylvania, Philadelphia, PA
Abstract:	Treatment failure rates for obesity are high, and a major factor in this failure is the difficulty in maintaining behavioral dietary change. In our investigation of the behavioral and neurobiological effects of reductions in dietary palatability, we have previously reported an increased emotionality and stress state in mice following withdrawal from a highly preferred high fat diet, and that these changes were linked with an increased risk for dietary relapse. The current study was designed to investigate the persistence of the behavioral vulnerability to dietary relapse, and to further elucidate the changes in stress and reward pathways in the brain that contribute to this behavior. Mice were exposed to a high fat diet for four weeks and examined in our dietary reinstatement paradigm up to 8 wks following diet withdrawal. We observed robust reinstatement behavior up to 6 wks post-withdrawal. In order to investigate gene expression changes in neural stress and reward pathways that might underlie dietary reinstatement, a separate cohort of mice was sacrificed prior to testing and specific brain regions micropunched for RT-PCR analysis. We hypothesized that changes in stress inputs from the central nucleus of the amygdala (CeA) and bed nucleus of the stria terminalis (BNST) to the ventral tegmental area (VTA) would interact with signals related to energy balance from the lateral hypothalamus to alter dopamine signaling and reinstatement behaviors. We found altered expression of corticotropin-releasing factor in the CeA and BNST, both of which project to the VTA. Dynorphin expression in the nucleus accumbens and kappa-opioid receptor expression in the VTA were increased, corresponding with reinstatement behaviors. In addition, we detected a robust reduction in expression of the leptin receptor in the VTA that was maintained for at least 8 wks following withdrawal, long after circulating plasma leptin levels had returned to baseline. The changes that we have observed in stress, reward, and energy balance pathways likely converge on the VTA to alter reward signaling, leading to an increased long-term risk of dietary relapse following diet withdrawal.
Disclosures:	S.L. Teegarden , None; T.L. Bale, None.
Support:	HRFF5-44071
	[Authors]. [Abstract Title]. Program No. XXX.XX. 2008 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2008. Online. 2008 Copyright by the Society for Neuroscience all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.


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