Neural activation patterns underlying basolateral amygdala influence on intra-accumbens opioid-driven consummatory versus appetitive high-fat feeding behaviors in the rat.
The present study explored the role of the amygdala in mediating a unique pattern of feeding behavior driven by intra-accumbens (intra-Acb) opioid activation in the rat. Temporary inactivation of the basolateral amygdala (BLA), via GABAA agonist muscimol administration prevents increased consumption following intra-Acb opioid administration of the selective μ-opioid agonist D-Ala2, NMe-Phe4, Glyol5-enkephalin (DAMGO), yet leaves food approach behaviors intact, particularly after consumption has ended. One interpretation is that inactivation of the BLA selectively blocks neural activity underlying DAMGO-driven consummatory (consumption) but not appetitive (approach) behaviors. The present experiments take advantage of this temporal dissociation of consumption and approach behaviors to investigate their associated neural activity. Following either intra-Acb saline or DAMGO administration, with or without BLA muscimol administration, rats were given 2-hr access to a limited amount of high-fat diet. Immediately following the feeding session, rats were sacrificed and brains assayed for neural activity patterns across critical brain regions known to regulate both appetitive and consummatory feeding behaviors. The results show that intra-Acb DAMGO administration increased c-Fos activation in orexin neurons within the perifornical area of the hypothalamus and that this increase in activation is blocked by BLA muscimol inactivation. Intra-Acb DAMGO administration significantly increased c-Fos activation within dopaminergic neurons of the ventral tegmental area, compared to saline controls, and BLA inactivation had no effect on this increase. Overall, these data provide underlying circuitry that may mediate the selective influence of the BLA on driving consummatory, but not appetitive, feeding behaviors in a model of hedonically driven feeding behavior.
Department of Psychological Sciences.
Kyle E
KE
Parker
Department of Psychological Sciences.
Matt P
MP
McCabe
Department of Psychological Sciences.
Howard W
HW
Johns
Christopher Bond Life Sciences Center.
Dane K
DK
Lund
Department of Biological Sciences.
Fiona
F
Odu
Christopher Bond Life Sciences Center.
Rishi
R
Sharma
Department of Neurology.
Mahesh M
MM
Thakkar
Christopher Bond Life Sciences Center.
D D W
DD
Cornelison
Department of Psychological Sciences.
Matthew J
MJ
Will
D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D001070:Appetitive Behavior / Q000187:drug effects / Q000502:physiology*; D066272:Basolateral Nuclear Complex / Q000187:drug effects / Q000502:physiology*; D059305:Diet, High-Fat; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000494:pharmacology; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology*; D058785:GABA-A Receptor Agonists / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology; D008297:Male; D009042:Motivation / Q000187:drug effects / Q000502:physiology; D009043:Motor Activity / Q000502:physiology; D009118:Muscimol / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009714:Nucleus Accumbens / Q000187:drug effects* / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000819:agonists / Q000378:metabolism; D017557:Ventral Tegmental Area / Q000187:drug effects / Q000502:physiology
D000701:Analgesics, Opioid; D058785:GABA-A Receptor Agonists; D016760:Proto-Oncogene Proteins c-fos; D017450:Receptors, Opioid, mu; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D009118:Muscimol