Opioid inhibition of kainic acid-induced scratching: Mediation by mu and sigma but not delta and kappa receptors

Scratching induced by intrathecal (IT) administration of kainic acid (0.5 nmol) to rats was inhibited by IT pretreatment with the selective mu agonists levorphanol (30 and 90 nmol), [D-Ala²,N-Met-Phe⁴, Gly⁵-ol]-enkaphalin (DAGO, 0.4 and 1.1 nmol), or morphine (90 nmol), the mixed mu-delta agonist [D-Ala²,D-Leu⁵]-enkaphalinamide (DADLE, 10 and 30 nmol), or the sigma/phencyclidine (PCP) agonists dextrorphan (90 nmol) or (+)-N-allyl-N-normetazocine ([+]-NAM, 90 nmol). The kappa agonists dynorphin (1.1 nmol) and ethylketocyclazocine (EKC, 90 nmol) had no significant effect, nor did the selective delta agonist [D-Pen²,D-Pen⁵]-enkaphalinamide (DPDPE, 90 nmol). The nonopioids (+)-3(3-hydroxyphenyl)-N-(1-propyl)piperidine([+])-3-PPP, 90 nmol) and PCP (90 nmol), selective for sigma and PCP sites, respectively, both antagonized kainic-induced scratching. Levorphanol- and DADLE-induced attenuation of scratching was partially antagonized by naltrexone. These findings suggest that opioid inhibition of kainic acid-induced scratching is mediated by classical mu receptors as well as sigma and PCP sites.