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Part of the book series: Perspectives in Antisense Science ((DARE,volume 1))

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Abstract

Opioid agonists produce their pharmacological effects by acting individually or in various combinations on the four different opioid receptor subtypes, δ, μ, κ and ε (Martin et al., 1976; Knapp et al., 1995; Porreca et al., 1995; Tseng, 1995). Stimulation of any one of these receptors by injection of the corresponding selective opioid receptor agonist produces analgesia and the analgesic effects produced by these agonists are selectively blocked by specific opioid receptor antagonists. Morphine and [D-Ala2,NMePhe4,Gly(ol)5]enkephalin (DAMGO) produce analgesia by interacting with μ-opioid receptors, [D-Ala2]deltorphin and [D-Pen2,5]enkephalin (DPDPE) evoke analgesia through an action on δ1- and δ2-opioid receptors, respectively, U50,488H causes analgesia via stimulation of κ-opioid receptors (Millan et al., 1989; Piercey and Einspahr, 1989) and β-endorphin given supraspinally produces analgesia through stimulation of ε-opioid receptors (Tseng, 1995). The resultant analgesic effects may be from either direct stimulation of opioid receptors in the spinal cord by intrathecal administration of opioids or activation of the descending pain control systems by supraspinally administered opioids.

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Tseng, L.F. (1998). Antisense Oligodeoxynucleotides as Specific Tools for Studying Opioid Receptor-Mediated Analgesia. In: McCarthy, M.M. (eds) Modulating Gene Expression by Antisense Oligonucleotides to Understand Neural Functioning. Perspectives in Antisense Science, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4933-8_7

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