We tend to develop a craving for certain substances more than others due to the innate reward mechanism in the central nervous system which is driven by limbic system mediated motivation. Understanding its neural basis is key to developing effective therapies for a broad spectrum of maladies such as drug addiction, obesity, anorexia nervosa and depression. The study of taste and the gustatory system gives us access to information about the reward mechanism as, unlike other complex motivations, its pathways are well documented, and the sensory stimulus is simple. Salt appetite is a biological drive triggered by a negative body sodium balance. This offers a unique model for investigating the central mechanisms of reward. Sodium salt taste further simplifies the situation, as the stimulus is only that of a single element, the sodium ion, and the sensory system involved is only that of taste. That sodium becomes rewarding only in the presence of a craving is a condition which can be easily reproduced in a laboratory setting. Salt appetite also has all the features of other complex motivations such as hunger, thirst etc.lt is crucial to know how this message reaches the limbic system from the parabrachial neucleus (PBN), the second gustatory relay station, to the ventral forebrain and changes the hedonic value. We propose, based on our pilot data, that the intermediate structure is the lateral hypothalamus (LH). Anatomical evidence does exist linking LH both to PBN and the ventral fore brain structures. Previous studies have shown the absence of sodium appetite in the presence of B/L PBN lesions as well as b/l LH lesions. Also, a dopamine overflow was noticed in the nucleus accumbans during salt ingestion in salt appetite. Release of dopamine in the NAC can be used as a forebrain index of reward. Whether this behavioral pattern and reward system are interrelated is yet to be elucidated. Thus, we aim to find the structure connecting PBN to the ventral forebrain and also to find a functional neuronal network to describe the reward related motivational behavior.We will use rats with asymmetrical central lesions in LH and PBN as experimental subjects. To measure the NAC dopamine overflow, microdialysis will be used and c Fos expression will be used as an immunohistochemical method to confirm our hypotheses as well as to find out the exact structures involved in order to investigate the reward related behavior which is a central puzzle in neuroscience.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32DC008937-03
Application #
7545900
Study Section
Communication Disorders Review Committee (CDRC)
Program Officer
Cyr, Janet
Project Start
2007-01-01
Project End
2009-12-31
Budget Start
2009-01-01
Budget End
2009-12-31
Support Year
3
Fiscal Year
2009
Total Cost
$59,402
Indirect Cost
Name
Pennsylvania State University
Department
Neurosciences
Type
Schools of Medicine
DUNS #
129348186
City
Hershey
State
PA
Country
United States
Zip Code
17033
Dayawansa, Samantha; Ruch, Stacey; Norgren, Ralph (2014) Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions. Am J Physiol Regul Integr Comp Physiol 306:R190-200
Dayawansa, S; Peckins, S; Ruch, S et al. (2011) Parabrachial and hypothalamic interaction in sodium appetite. Am J Physiol Regul Integr Comp Physiol 300:R1091-9