NEUROANATOMICAL PATTERNS OF FOS-LIKE IMMUNOREACTIVITY INDUCED BY A PALATABLE MEAL AND MEAL-PAIRED ENVIRONMENT IN SALINE-TREATED AND NALTREXONE-TREATED RATS

Authors
Citation
Th. Park et Kd. Carr, NEUROANATOMICAL PATTERNS OF FOS-LIKE IMMUNOREACTIVITY INDUCED BY A PALATABLE MEAL AND MEAL-PAIRED ENVIRONMENT IN SALINE-TREATED AND NALTREXONE-TREATED RATS, Brain research, 805(1-2), 1998, pp. 169-180
Citations number
64
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
805
Issue
1-2
Year of publication
1998
Pages
169 - 180
Database
ISI
SICI code
0006-8993(1998)805:1-2<169:NPOFII>2.0.ZU;2-E
Abstract
Opioid antagonists block the positive hedonic response to food taste a nd are potent inhibitors of palatability-driven feeding. However, the specific brain regions within which opioid peptide secretion contribut es to the maintenance of palatability-driven feeding have not been cle arly established. In the present study, c-Fos immunohistochemistry was used to identify regions rostral to the hindbrain that display cellul ar activation in response to a palatable meal and the meal-paired envi ronment. Further, it was determined whether any of the cellular respon ses could be prevented by pretreating animals with naltrexone. Twenty brain regions known to be involved in gustation, appetite and reward f unctions were examined. Ingestion of the palatable meal (3.0 g of 30% shortening, 20% sucrose and 50% powdered Purina rat chow) increased Fo s-like immunoreactivity (FLI) in lateral hypothalamus (LH), ventral te gmentum (VTA) and medial preoptic area (MPOA), and decreased FLI in th e habenula (Hab). The meal-paired environment increased FLI in the VTA and nucleus accumbens shell (NAC shell). Naltrexone (1.0 mg/kg, i.p.) did not block consumption of the small meal but did prevent all of th e distinctive increases in FLI induced by the meal and meal-paired env ironment. Since naltrexone, alone, increased FLI in VTA, NAC shell, ce ntral amygdala (ceA) and laterodorsal bed nucleus of the stria termina lis (BSTLD), the blunting of ingestion reward by naltrexone may result from direct or transsynaptic activating effects on opponent neuronal activity within this highly interconnected set of structures that medi ate and modulate reward. (C) 1998 Elsevier Science B.V. All rights res erved.