Lateral hypothalamus, nucleus accumbens, and ventral pallidum roles in eating and hunger: interactions between homeostatic and reward circuitry

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.

Making the Case for ‘Power Abuse Disorder' as a Nosologic Entity

“…To conclude our brief overview of the current hypotheses regarding the role of the dopamine system (1) in motivated behavior, that is, in the seeking of attractive stimuli or avoidance of aversive stimuli; and (2) consummation/consumption of coveted stimuli, some researchers emphasize that accumbal activation can be separated into signaling a dopamine-independent “hedonic impact” or “liking” of a stimulus and signaling its “motivational salience,” that is, the “wanting” such an attractive/appetitive/positively reinforcing stimulus elicits, in a dopamine-dependent manner [27]. For an illustration of the psychologic constructs involved in explaining “reward” and “reinforcement,” the reader is referred to [21].…”

“…Another nonpharmacologic stimulus that may engender addictive behavior, internet gaming, is already on its way to be incorporated into mental disorder compendia, as evidenced by its inclusion as a “condition for further study” in the DSM5 [25]. To emphasize, any motivated behavior, including food seeking and consumption [27], carries the risk of becoming addictive, with the nucleus accumbens (see, e.g., [10,17,18,19,20,21,22,23]) and, possibly, the whole accumbens corridor [10,28,29] as the central neuroanatomic hot spot of the motivational neuronetwork (reward pathways) and dopamine as the major neurotransmitter driving motivated behavior. Interestingly, food and power share the paradox of being both essential for our survival as well as becoming extremely harmful for us if abused.…”

Homeostasis Meets Motivation in the Battle to Control Food Intake

“…1). This system is critically involved in generating motivated behaviors, including feeding (Kelley et al, 2005;Wise, 2006;Castro et al, 2015). In addition, hypothalamic and thalamic nuclei implicated in arousal, consumption and hunger; the paraventricular thalamic (PVT) nucleus, lateral hypothalamus (LH), and the ventromedial hypothalamus, respectively, interact closely with neural nodes of the MCL (Fig.…”

Roles of “Wanting” and “Liking” in Motivating Behavior: Gambling, Food, and Drug Addictions

“…1). The "liking" and "wanting" systems in the brain have some structural and neurochemical overlap, but also separate substrates (Berridge et al , 2010Castro et al 2015). While both systems are contained within certain common mesolimbic structures, the "liking" components, or hedonic "hot spots," are only small subregions of these greater mesolimbic structures, including the nucleus accumbens and ventral pallidum Berridge et al 2010).…”