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Involvement of dynorphin in immobilization stress-induced antinociception in the mouse
1Hallym University, College of Medicine, Institute of Natural Medicine, Department of Pharmacology, Chunchon, Kangwon Do, 200-702, South Korea.hwsuh@sun.hallym.ac.kr
The effect of antiserum against [Met(5)]-enkephalin, [Leu(5)]-enkephalin, beta-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 assay. Immobilization of the mouse increased inhibition of the tail-flick response at least 1 h. The i.c.v. or i.t. injection with antiserum against dynorphin A-(1-13) at the dose of 200 microg significantly attenuated immobilization-induced inhibition of the tail-flick response. However, antiserum against [Met(5)]-enkephalin, [Leu(5)]-enkephalin, or beta-endorphin did not affect the immobilization stress-induced antinociception. Furthermore, i.c.v. or i.t. injection with nor-binaltorphimine (Nor-BNI; from 1 to 20 microg) effectively inhibited immobilization stress-induced inhibition of the tail-flick response in a dose-dependent manner. However, beta-FNA (from 0.5 to 2 microg) or naltrindole (from 1 to 20 microg) administered i.c.v. or i.t. did not affect immobilization stress-induced antinociception. Our results suggest that supraspinally and spinally located dynorphin appears to be involved in the production of immobilization stress-induced antinociception via stimulating kappa-opioid receptors.
The effect of antiserum against [Met(5)]-enkephalin, [Leu(5)]-enkephalin, beta-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 assay. Immobilization of the mouse increased inhibition of the tail-flick response at least 1 h. The i.c.v. or i.t. injection with antiserum against dynorphin A-(1-13) at the dose of 200 microg significantly attenuated immobilization-induced inhibition of the tail-flick response. However, antiserum against [Met(5)]-enkephalin, [Leu(5)]-enkephalin, or beta-endorphin did not affect the immobilization stress-induced antinociception. Furthermore, i.c.v. or i.t. injection with nor-binaltorphimine (Nor-BNI; from 1 to 20 microg) effectively inhibited immobilization stress-induced inhibition of the tail-flick response in a dose-dependent manner. However, beta-FNA (from 0.5 to 2 microg) or naltrindole (from 1 to 20 microg) administered i.c.v. or i.t. did not affect immobilization stress-induced antinociception. Our results suggest that supraspinally and spinally located dynorphin appears to be involved in the production of immobilization stress-induced antinociception via stimulating kappa-opioid receptors.