TY - JOUR T1 - β-Endorphin-Induced Feeding: Pharmacological Characterization Using Selective Opioid Antagonists and Antisense Probes in Rats JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 590 LP - 596 VL - 297 IS - 2 AU - Robert M. Silva AU - Maria M. Hadjimarkou AU - Grace C. Rossi AU - Gavril W. Pasternak AU - Richard J. Bodnar Y1 - 2001/05/01 UR - http://jpet.aspetjournals.org/content/297/2/590.abstract N2 - Ventricular administration of the opioid βEND induces feeding in rats. Since its pharmacological characterization has not been fully identified, the present study examined whether equimolar doses of general and selective opioid antagonists as well as AS ODN opioid probes altered spontaneous daytime feeding over a 4-h time course elicited by βEND. βEND-induced feeding was significantly reduced by moderate (20–40-nmol, i.c.v.) doses of general (naltrexone) opioid antagonists, and lower (0.5–40-nmol) doses of selective μ (β-funaltrexamine)-antagonists. Correspondingly, AS ODN probes directed against either exons 1, 3, or 4, but not exon 2, of the μ-opioid receptor clone reduced βEND-induced feeding; a missense ODN control probe was ineffective. The δ-antagonist Nti (20–40 nmol) reduced βEND-induced feeding to a lesser degree, and AS ODN probes targeting exon 1, but not 2 or 3, of the δ-opioid receptor clone significantly reduced βEND-induced feeding. Although the selective κ1-receptor antagonist NBNI (20–40 nmol) significantly reduced βEND-induced feeding, this response was not altered by AS ODN probes directed against either exons 1, 2, or 3 of either the KOR-1 clone or the κ3-like opioid receptor clone. These converging antagonist and AS ODN data firmly implicate the μ-opioid receptor in the mediation of βEND-induced feeding. The relative lack of convergence between the lesser effectiveness of Nti and NBNI in reducing βEND-induced feeding, and the lack of effectiveness of their corresponding AS ODN probes suggest that δ- and κ-receptors play a minimal role in the mediation of this response. The American Society for Pharmacology and Experimental Therapeutics ER -