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High-probability grants
According to our matching algorithm, Sharif A. Taha is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2008 — 2009 |
Taha, Sharif A. |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Appetitive/Aversive Encoding in the Nucleus Accumbens
[unreadable] DESCRIPTION (provided by applicant): Our long-term goal is to understand function in brain circuits which regulate reward-seeking and feeding behaviors. Brain circuits which regulate these behaviors are also implicated in the control of defensive responding elicited by threat or aversive stimuli; however, the manner in which these circuits coordinate competing appetitive and defensive behaviors is not understood. Pharmacological inhibition of neural firing in the medial shell region of the nucleus accumbens (NAcc) has been shown to dramatically elevate food intake in satiated animals and to increase reward-seeking behaviors; conversely, increases in neural firing in this region suppress food intake in hungry animals. The neural firing patterns which underlie these behavioral effects are poorly understood. Electrophysiological experiments in behaving animals have demonstrated that the predominant pattern of neural firing encountered in recordings from the NAcc is of an inhibition of neural firing occurring prior to and during feeding behavior. In the proposed experiments, we will test the hypothesis that NAcc neurons possessing this firing pattern play an important role in the normal control of appetitive and feeding behavior, and that inhibition of firing in these neurons underlies the behavioral effects of pharmacological inhibition of firing in the NAcc shell. In Specific Aim 1, we will examine the core/shell distribution of this firing pattern to determine if it is predominantly localized to the NAcc shell. In Specific Aim 2 we will determine if this firing pattern is correlated with appetitive behaviors. Specifically, we will measure and compare firing in this class of neurons during reward seeking to determine 1) if inhibition onset is synchronous with the onset of goal-directed locomotor approach behaviors and 2) if inhibition of neural firing occurs specifically during goal-directed locomotor and operant behaviors. In Specific Aim 3 we will test the response properties of these NAcc neurons during presentation of an aversive cue, to test the hypothesis that aversive stimuli increase firing rate in these neurons, with the behavioral effect of suppressing appetitive/feeding behaviors when threat stimuli arise. These studies are relevant to human health because they will aid in elucidating function in neural circuits that underlie initiation of goal-directed behavior, and importantly, in identifying neural mechanisms mediating suppression of reward-seeking behaviors. Neural dysfunction in disorders of motivation such as addiction is characterized by an inability to inhibit drug-seeking behaviors despite the damaging consequences of continued drug use. The experiments outlined will aid in understanding function in neural circuits importantly implicated in addiction. Addiction is characterized by an inability to suppress drug-seeking despite the devastating negative consequences of continued drug use. Understanding brain circuits which regulate natural reward-seeking behaviors is an important step in understanding neural changes underlying addiction. The proposed experiments will elucidate function in brain circuits importantly implicated in initiating reward-seeking behavior. [unreadable] [unreadable] [unreadable]
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2012 — 2013 |
Taha, Sharif A. |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Opioid Modulation of Neural Encoding of Motivation and Reward
DESCRIPTION (provided by applicant): Our long-term goal is to understand the contribution of neural reward circuits to control of food intake during normal consumption as well as in pathologies that incorporate binge eating. We are specifically interested in how opioid signaling within reward circuits, particularly in the shell of the nucleus accumbens (sNAcc), mediates binge-like food intake. Stimulation of mu opioid receptors (MORs) in the sNAcc induces voracious feeding and sNAcc opioid receptor and ligand expression is altered in rat models of diet-induced binge eating. However, the mechanisms through which sNAcc MOR stimulation causes hyperphagia, and how diet-induced changes in this circuit contribute to binge eating behavior, remain poorly understood. In previous studies, we characterized two firing patterns in sNAcc neurons that we hypothesize play important and distinct roles in processing of taste hedonics and controlling appetitive food-seeking behavior. Our data suggests that the first of these firing patterns encodes palatability, while the second serves to permissively gate food-seeking behavior (and subsequent consumption) through a disinhibition mechanism. In the present proposal, we will test the hypothesis that distinct effects of sNAcc MOR stimulation on these firing patterns act to increase palatability-induced hyperphagia and food-seeking appetitive behaviors through signaling in segregated anatomical pathways. We further hypothesize that diet-induced binge eating arises specifically through sensitization of opioid signaling in the neural pathway mediating appetitive food-seeking, rather than through changes in pathways processing palatability. To address these hypotheses, we will use a combination of in vivo electrophysiological and pharmacological approaches to characterize the effects of sNAcc MOR manipulations on firing in efferent targets of the sNAcc. We will investigate interactions between the sNAcc and target regions using simultaneous electrode array recordings and cross-correlation techniques to characterize functional connectivity between these regions. Finally, we will characterize electrophysiological and pharmacological changes occurring in this circuit in a rat model of diet-induced binge eating. We anticipate that these experiments will provide important insights into the mechanisms underlying hyperphagia caused by sNAcc MOR stimulation and diet-induced binge eating. These experiments will lead to greater understanding of neural-circuit mechanisms underlying compulsive food intake, and are thus highly relevant in developing novel therapeutic interventions for eating disorders such as bulimia nervosa. PUBLIC HEALTH RELEVANCE: Eating disorders incorporating binge eating are commonly occurring diseases with devastating effects on health. Understanding the neural circuits controlling food intake, and how changes in these circuits lead to compulsive binge eating, is critical to developing novel therapies for treatment of associated disorders. The proposed research will advance our understanding of the mechanisms through which brain reward circuits control binge-like intake of highly palatable foods. This research will thus advance our understanding of root causes of compulsive binge eating in disorders such as bulimia nervosa.
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