Measuring food reward value in humans

ARTICLE IN PRESS 304

Abstracts / Appetite 49 (2007) 272–341

Effects of cross-wiring the lingual taste nerves on quinine-stimulated Fos-immunoreactivity in the rat parabrachial nucleus C.T. KINGa, M. GARCEAb, A.C. SPECTORb. a

Department of Psychology, Stetson University, DeLand, FL 32723, USA. bDepartment of Psychology and Center for Smell and Taste, Gainesville, FL 32611, USA By surgically cross-wiring the taste nerves into non-native receptor fields (the glossopharyngeal (GL) into the anterior tongue (GLc/AT) or the chorda tympani (CT) into the posterior tongue (CTc/PT), we showed previously that unconditioned quinine-induced gaping and neuronal activity, assessed by c-Fos immunohistochemistry, in the rostral nucleus of the solitary tract (rNST), were fully and partially restored, respectively, only if the PT taste receptor field was reinnervated; the particular taste nerve supplying the input was inconsequential to the recovery of function. These findings suggested that a cluster of Fos-expressing cells in the most rostral pole of the rNST may be importantly associated with neural circuits involved in the generation of unconditioned taste-triggered rejection reflexes. We are now examining in these same animals the distribution of Fos-positive neurons in the waist area of the parabrachial nucleus (PBN), the second obligatory central relay in the ascending rodent gustatory system. Preliminary data indicate that quinine-stimulated controls (N=3) and animals with regeneration of the GL into its native PT receptor field (N=2) show robust neural activity (121.0733.5 and 136.576.5 Fos-positive neurons, respectively) compared with water-stimulated controls (N=3, 31.676.1). The CTc/PT crosswiring (N=3) appears to be more effective in maintaining quinine-stimulated neural activity in the waist area (81.3718.0) than the GLc/AT cross-wiring (N=3, 30.078.6). Presently, we are analyzing the remaining subjects and other PBN subdivisions to explore further the remarkable ability of the central gustatory to adapt to peripherally reorganized neural taste input. Supported by NIH-R01-DC01628. 10.1016/j.appet.2007.03.108

reinforcement schedule (CRF). On CRF, intake of the sweet yogurt (782 g762 SE) was 208 g767 SE higher than non-sweet yogurt (po0.05). On PR, neither intake nor number of reinforcements differed between sweet and non-sweet shakes. However, intake difference between sweet and non-sweet shakes was correlated with VAS-rated liking difference (R=0.4, p=0.03), which was significantly (p=0.01) lower on PR (26/ 150 mm) than CRF (57/150 mm). For humans, intake on a CRF task appears to be a better measure of reward value for sweet and non-sweet yogurts than work on a PR task. The effort required to obtain the drink on the PR task appeared to devalue its reward, and other schedule parameters need to be investigated. Support: DK26687 (NYORC), DK31135 (AS). 10.1016/j.appet.2007.03.109

Intraperitoneal (ip) bacterial lipopolysaccharide (LPS) elicits rapid, graded increases in c-Fos expression in the raphe pallidus nucleus (Rpa) and central nucleus of the amygdala (cea) in male rats B.S. KOPF, N. GEARY, W. LANGHANS, L. ASARIAN.

Institute of Animal Sciences, ETH Zurich, 8603 Schwerzenbach, Switzerland

Measuring food reward value in humans H.R. KISSILEFFa,b, S.J.

M NALLYa,b, R. GORDONa,b, M. GONDEK-BROWNa,b, J. FARKASa,b, A. SCLAFANIa,b. aNew York Obesity Research Center, St. Luke’s/Roosevelt Hospital, Columbia University, New York, NY 10025 USA. bBrooklyn College-CUNY, Brooklyn, NY 11210, USA Progressive ratio (PR) licking is a sensitive measure of sucrose reward in rats (Sclafani & Ackroff, 2003). A human analog of the PR licking task was created by having subjects (seven men and eight women) pull and suck on a straw for progressively longer time intervals (5-sincrements) to obtain 2-s access to an artificially sweetened (Equals) or non-sweet yogurt shake on separate days. On two other days, each yogurt was available on a continuous

LPS, a potent activator of the innate immune system, is commonly used to investigate the acute phase response to infection, including anorexia. We investigated the association between the intensity of LPS anorexia and (1) the activation of brain sites initially responding to LPS, measured with c-Fos expression, and (2) co-localization of c-Fos responses with tyrosine hydroxylase (TH), a marker of catecholaminergic (CA) neurons, in the A1 noradrenergic cells (A1). Male Long-Evans rats received 1 ml/kg ip injections of 0, 12.5 or 100 mg/kg LPS at dark onset. Food intake was measured in one set of rats, and cFos and its co-localization with TH in another, unfed set 90 min post-injection. LPS reduced 120 min food intake in a significantly dose-related manner. LPS increased c-Fos expression in the A1, RPa, nucleus tractus solitarius, paraventricular nucleus, and CeA. C-Fos expression was dose-related, however, only in the RPa and CeA. LPS induced c-Fos in TH-positive neurons in the A1, but this was not dose-related. These results suggest that the doserelated effect of LPS on food intake (1) may originate in differential neuronal processing of LPS-induced signals in the RPa or CeA and (2) does not originate in CA neurons in the A1. 10.1016/j.appet.2007.03.110