TY - JOUR
T1 - Opioid receptor involvement in food deprivation-induced feeding
T2 - Evaluation of selective antagonist and antisense oligodeoxynucleotide probe effects in mice and rats
AU - Hadjimarkou, M. M.
AU - Singh, A.
AU - Kandov, Y.
AU - Israel, Y.
AU - Pan, Y. X.
AU - Rossi, G. C.
AU - Pasternak, G. W.
AU - Bodnar, Richard J.
PY - 2004/12
Y1 - 2004/12
N2 - Central administration of general and selective opioid receptor subtype antagonists in the rat has revealed a substantial role for μ, a moderate role for κ, and a minimal role for δ receptors in the mediation of deprivation-induced feeding. Antisense probes directed against the κ opioid receptor (KOP), nociceptin opioid receptor (NOP), and δ opioid receptor (DOP) genes in rats result in reductions similar to κ and δ antagonists, whereas antisense probes directed against the μ opioid receptor (MOP) gene produced modest reductions relative to μ antagonists, suggesting that isoforms of the MOP gene may mediate deprivation-induced feeding. Since these isoforms were initially identified in mice, the present study compared the effects of general and selective opioid receptor antagonists on deprivation-induced feeding in rats and mice and antisense probes directed against exons of the MOP, DOP, KOP, and NOP genes on deprivation-induced feeding in the mouse, Food-deprived (12 and 24 h) rats and mice displayed similar profiles of reductions in deprivation-induced feeding following general, μ, and κ opioid antagonists. In contrast, mice, but not rats, displayed reductions in deprivation-induced intake following δ antagonism as well as DOP antisense probes, suggesting a species-specific role for the δ receptor. Antisense probes directed against the KOP and NOP genes also reduced deprivation-induced intake in mice in a manner similar to κ antagonism. However, the significant reductions in deprivation - induced feeding following antisense probes directed against either exons 2, 4, 7, 8, or 13 of the MOP gene were modest compared with μ antagonism, suggesting a role for multiple A-mediated mechanisms.
AB - Central administration of general and selective opioid receptor subtype antagonists in the rat has revealed a substantial role for μ, a moderate role for κ, and a minimal role for δ receptors in the mediation of deprivation-induced feeding. Antisense probes directed against the κ opioid receptor (KOP), nociceptin opioid receptor (NOP), and δ opioid receptor (DOP) genes in rats result in reductions similar to κ and δ antagonists, whereas antisense probes directed against the μ opioid receptor (MOP) gene produced modest reductions relative to μ antagonists, suggesting that isoforms of the MOP gene may mediate deprivation-induced feeding. Since these isoforms were initially identified in mice, the present study compared the effects of general and selective opioid receptor antagonists on deprivation-induced feeding in rats and mice and antisense probes directed against exons of the MOP, DOP, KOP, and NOP genes on deprivation-induced feeding in the mouse, Food-deprived (12 and 24 h) rats and mice displayed similar profiles of reductions in deprivation-induced feeding following general, μ, and κ opioid antagonists. In contrast, mice, but not rats, displayed reductions in deprivation-induced intake following δ antagonism as well as DOP antisense probes, suggesting a species-specific role for the δ receptor. Antisense probes directed against the KOP and NOP genes also reduced deprivation-induced intake in mice in a manner similar to κ antagonism. However, the significant reductions in deprivation - induced feeding following antisense probes directed against either exons 2, 4, 7, 8, or 13 of the MOP gene were modest compared with μ antagonism, suggesting a role for multiple A-mediated mechanisms.
UR - http://www.scopus.com/inward/record.url?scp=10044269659&partnerID=8YFLogxK
U2 - 10.1124/jpet.104.071761
DO - 10.1124/jpet.104.071761
M3 - Article
C2 - 15333676
AN - SCOPUS:10044269659
SN - 0022-3565
VL - 311
SP - 1188
EP - 1202
JO - Journal of Pharmacology and Experimental Therapeutics
JF - Journal of Pharmacology and Experimental Therapeutics
IS - 3
ER -