Abstract
The current proposal takes a circuit-based approach to investigate how the gustatory cortex (GC) processes the
hedonic value (or palatability) of a food in cooperation with the basolateral amygdala (BLA) and lateral
hypothalamus (LH). This complex circuit approach is taken because the control of ingestion is a complicated
process: while physiological needs (e.g., hunger, thirst) exert an important force on consumption, the hedonic
value of a taste plays a powerful, potentially competing role; in fact, we often eat or drink not to satisfy
physiological needs but to fulfill the desire to consume palatable food—a desire that, in extreme cases, may
eventually lead to disorders such as binge eating and bulimia nervosa, severe social issues that affect millions
of people a year in the United States. Our work has established that GC, the cortical projection of the central
gustatory system, plays a pivotal role in processing the hedonic value of a taste stimulus: GC taste responses
show 2 temporally separated firing epochs, the first representing taste identity (here, Epoch 1) and the second
epoch reflecting the hedonic value conveyed by the taste (Epoch 2); furthermore, this activity not only reflects
palatability but plays a role in causing it—the onset of Epoch 2 predicts the timing of taste-evoked orofacial
responses, and inhibition of GC significantly perturbs production of those responses. The current work will extend
these findings by exploring the rich reciprocal connections between GC and BLA and LH, subcortical areas in
which taste responses also show epoch-like firing activity. I hypothesize that palatability-related firing in GC
requires inputs from BLA and/or LH. To test this hypothesis, I will directly examine how optogenetic silencing of
projections from BLA and/or LH influence GC taste responses (Aim 1) and learning-related changes in
palatability (Aim 2, conditioned taste aversion or CTA). Finally, in Aim 3, with the use of a genetically engineered
rat model (ChAT::cre+ rats), I will evaluate the influence of cholinergic signaling perturbation on naïve and
learning-related palatability behavior and attendant neural responses, thus deepening my search for specific
pathways responsible for the processing of palatability. Together, this research project will enrich our
understanding of neural control of palatability-mediated consumption, based on which we may identify more
effective treatment and prevention strategies for eating disorders.