Abstract
The study of the neural bases of eating behavior, hunger, and reward has consistently implicated the lateral hypothalamus (LH) and its interactions with mesocorticolimbic circuitry, such as mesolimbic dopamine projections to nucleus accumbens (NAc) and ventral pallidum (VP), in controlling motivation to eat. The NAc and VP play special roles in mediating the hedonic impact (“liking”) and motivational incentive salience (“wanting”) of food rewards, and their interactions with LH help permit regulatory hunger/satiety modulation of food motivation and reward. Here, we review some progress that has been made regarding this circuitry and its functions: the identification of localized anatomical hedonic hotspots within NAc and VP for enhancing hedonic impact; interactions of NAc/VP hedonic hotspots with specific LH signals such as orexin; an anterior-posterior gradient of sites in NAc shell for producing intense appetitive eating vs. intense fearful reactions; and anatomically distributed appetitive functions of dopamine and mu opioid signals in NAc shell and related structures. Such findings help improve our understanding of NAc, VP, and LH interactions in mediating affective and motivation functions, including “liking” and “wanting” for food rewards.
Highlights
Taste Reactivity as a Measure of Hedonic ImpactTo ascertain whether or not lateral hypothalamus (LH) stimulation did enhance a taste signal, a more direct measure of taste hedonic impact was needed, such as the affective taste reactivity test
The study of the neural bases of eating behavior, hunger, and reward has consistently implicated the lateral hypothalamus (LH) and its interactions with mesocorticolimbic circuitry, such as mesolimbic dopamine projections to nucleus accumbens (NAc) and ventral pallidum (VP), in controlling motivation to eat
We review some progress that has been made regarding this circuitry and its functions: the identification of localized anatomical hedonic hotspots within NAc and VP for enhancing hedonic impact; interactions of NAc/VP hedonic hotspots with specific LH signals such as orexin; an anterior-posterior gradient of sites in NAc shell for producing intense appetitive eating vs. intense fearful reactions; and anatomically distributed appetitive functions of dopamine and mu opioid signals in NAc shell and related structures
Summary
To ascertain whether or not LH stimulation did enhance a taste signal, a more direct measure of taste hedonic impact was needed, such as the affective taste reactivity test. Bitter tasting quinine or highly concentrated sodium chloride both elicit similar aversive ‘‘disgust’’ reaction patterns, and both are avoided compared to water (Berridge et al, 1984) Another line of evidence supporting a hedonic interpretation comes from observations that a single taste sensation can evoke quite different orofacial reactions under different conditions relevant to its palatability. When rats with central amygdala lesions are tested in taste reactivity, they still show an affective change in orofacial reactions from ‘‘disgust’’ to ‘‘liking’’ patterns (Galaverna et al, 1993) This dissociation indicates that the hedonic alliesthesia shift remains intact, but no longer controls any appetitive or consummatory aspect of ingestion (Galaverna et al, 1993; Seeley et al, 1993). The basic circuitry needed to generate oromotor facial patterns is contained within the brainstem, the forebrain imposes hierarchical control over affective aspects of these reaction patterns
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
