title: Central amygdala opioid transmission is necessary for increased high-fat intake following 24-h food deprivation, but not following intra-accumbens opioid administration.
abstract: Previous research has demonstrated a dissociation of certain neural mediators that contribute to the increased consumption of a high-fat diet that follows intra-accumbens (Acb) administration of μ-opioid receptor agonists vs. 24-h food deprivation. These two models, both which induce rapid consumption of the diet, have been shown to involve a distributed corticolimbic circuitry, including the amygdala. Specifically, the central amygdala (CeA) has been shown to be involved in high-fat feeding within both opioid and food-deprivation driven models. The present experiments were conducted to examine the more specific role of CeA opioid transmission in mediating high-fat feeding driven by either intra-Acb administration of the μ-opioid agonist d-Ala2-NMe-Phe4-Glyol5-enkephalin (DAMGO) or 24-h home cage food deprivation. Injection of DAMGO into the Acb (0.25 μg/0.5 μl/side) increased consumption of the high-fat diet, but this feeding was unaffected by administration of opioid antagonist, naltrexone (5 μg/0.25 μl/side) administered into the CeA. In contrast, intra-CeA naltrexone administration attenuated high-fat intake driven by 24-h food deprivation, demonstrating a specific role for CeA opioid transmission in high-fat consumption. Intra-CeA naltrexone administration alone had no effect on baseline feeding levels within either feeding model. These findings suggest that CeA opioid transmission mediates consumption of a palatable high-fat diet driven by short-term negative-energy balance (24-h food deprivation), but not intra-Acb opioid receptor activation.
authors.affiliation: Department of Psychology, Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA. Electronic address: kepfg4@mail.mizzou.edu.
authors.forename: Kyle E
authors.initials: KE
authors.lastname: Parker
authors.affiliation: Department of Psychology, Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA.
authors.forename: Howard W
authors.initials: HW
authors.lastname: Johns
authors.affiliation: Department of Psychology, Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA.
authors.forename: Ted G
authors.initials: TG
authors.lastname: Floros
authors.affiliation: Department of Psychology, Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, MO 65211, USA.
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Will
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000701:Analgesics, Opioid / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D059305:Diet, High-Fat; D004435:Eating / Q000187:drug effects / Q000502:physiology; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000008:administration & dosage / Q000494:pharmacology; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology*; D005508:Food Deprivation / Q000502:physiology*; D008297:Male; D008845:Microinjections; D009271:Naltrexone / Q000008:administration & dosage / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D009714:Nucleus Accumbens / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013997:Time Factors
chemical_list: D000701:Analgesics, Opioid; D009292:Narcotic Antagonists; D017450:Receptors, Opioid, mu; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D009271:Naltrexone
keywords: Central amygdala; DAMGO; Feeding; Food deprivation; High-fat diet; Nucleus accumbens