Ryan A Selleck1, Brian A Baldo2. 1. Department of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine & Science, 3333 Green Bay Rd., North Chicago, IL, 60064, USA. 2. Department of Psychiatry, University of Wisconsin-Madison School of Medicine and Public Health, 6001 Research Park Blvd., Madison, WI, 53719, USA. babaldo@wisc.edu.
Abstract
RATIONALE: Whereas reward-modulatory opioid actions have been intensively studied in subcortical sites such as the nucleus accumbens (Acb), the role of cortical opioid transmission has received comparatively little attention. OBJECTIVES: The objective of this study is to describe recent findings on the motivational actions of opioids in the prefrontal cortex (PFC), emphasizing studies of food motivation and ingestion. PFC-based opioid effects will be compared/contrasted to those elicited from the Acb, to glean possible common functional principles. Finally, the motivational effects of opioids will be placed within a network context involving the PFC, Acb, and hypothalamus. RESULTS: Mu-opioid receptor (μ-OR) stimulation in both the Acb and PFC induces eating and enhances food-seeking instrumental behaviors; μ-OR signaling also enhances taste reactivity within a highly circumscribed zone of medial Acb shell. In both the Acb and PFC, opioid-sensitive zones are aligned topographically with the sectors that project to feeding-modulatory zones of the hypothalamus and intact glutamate transmission in the lateral/perifornical (LH-PeF) hypothalamic areas is required for both Acb- and PFC-driven feeding. Conversely, opioid-mediated feeding responses elicited from the PFC are negatively modulated by AMPA signaling in the Acb shell. CONCLUSIONS: Opioid signaling in the PFC engages functionally opposed PFC➔hypothalamus and PFC➔Acb circuits, which, respectively, drive and limit non-homeostatic feeding, producing a disorganized and "fragmented" pattern of impulsive food-seeking behaviors and hyperactivity. In addition, opioids act directly in the Acb to facilitate food motivation and taste hedonics. Further study of this cortico-striato-hypothalamic circuit, and incorporation of additional opioid-responsive telencephalic structures, could yield insights with translational relevance for eating disorders and obesity.
RATIONALE: Whereas reward-modulatory opioid actions have been intensively studied in subcortical sites such as the nucleus accumbens (Acb), the role of cortical opioid transmission has received comparatively little attention. OBJECTIVES: The objective of this study is to describe recent findings on the motivational actions of opioids in the prefrontal cortex (PFC), emphasizing studies of food motivation and ingestion. PFC-based opioid effects will be compared/contrasted to those elicited from the Acb, to glean possible common functional principles. Finally, the motivational effects of opioids will be placed within a network context involving the PFC, Acb, and hypothalamus. RESULTS: Mu-opioid receptor (μ-OR) stimulation in both the Acb and PFC induces eating and enhances food-seeking instrumental behaviors; μ-OR signaling also enhances taste reactivity within a highly circumscribed zone of medial Acb shell. In both the Acb and PFC, opioid-sensitive zones are aligned topographically with the sectors that project to feeding-modulatory zones of the hypothalamus and intact glutamate transmission in the lateral/perifornical (LH-PeF) hypothalamic areas is required for both Acb- and PFC-driven feeding. Conversely, opioid-mediated feeding responses elicited from the PFC are negatively modulated by AMPA signaling in the Acb shell. CONCLUSIONS: Opioid signaling in the PFC engages functionally opposed PFC➔hypothalamus and PFC➔Acb circuits, which, respectively, drive and limit non-homeostatic feeding, producing a disorganized and "fragmented" pattern of impulsive food-seeking behaviors and hyperactivity. In addition, opioids act directly in the Acb to facilitate food motivation and taste hedonics. Further study of this cortico-striato-hypothalamic circuit, and incorporation of additional opioid-responsive telencephalic structures, could yield insights with translational relevance for eating disorders and obesity.
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