Involvement of dynorphin in immobilization stress-induced antinociception in the mouse

The effect of antiserum against [Met(5)]-enkephalin, [Leu(5)]-enkephalin, b eta-endorphin, or dynorphin A-(1-13) administered intracerebroventricularly (i.c.v.) or intrathecally (i.t.) on immobilization-induced antinociception was studied in ICR mice. Antinociception was assessed by the tail-flick as say. Immobilization of the mouse increased inhibition of the tail-flick res ponse at least 1 h. The i.c.v. or i.t. injection with antiserum against dyn orphin A-(1-13) at the dose of 200 mu g significantly attenuated immobiliza tion-induced inhibition of the tail-flick response. However, antiserum agai nst [Met(5)]-enkephalin, [Leu(5)]-enkephalin, or beta-endorphin did not aff ect the immobilization stress-induced antinociception. Furthermore, i.c.v. or i.t. injection with nor-binaltorphimine (Nor-BNI; from I to 20 mu g) eff ectively inhibited immobilization stress-induced inhibition of the tail-fli ck response in a dose-dependent manner. However, beta-FNA (from 0.5 to 2 mu g) or naltrindole (from 1 to 20 mu g) administered i.c.v. or i.t. did not affect immobilization stress-induced antinociception. Our results suggest t hat supraspinally and spinally located dynorphin appears to be involved in the production of immobilization stress-induced antinociception via stimula ting kappa-opioid receptors. (C) 2000 Published by Elsevier Science BN.