Antinociceptive Effect of Smilaxin B Administered Intracerebroventricularly in the Mouse

Abstract

We examined the antinociceptive effect of smilaxin B administered intracerebroventricularly (i.c.v.) in ICR mice. The tail-flick test was used as an analgesic assay. Smilaxin B showed a strong antinociceptive effect in a dose-dependent manner. Sulfated cholecystokinin (CCK-8s, 0.5 ng), muscimol (50 ng), or MK-801 [(±)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate, 1 µg] injected i.c.v. significantly reduced inhibition of the tail-flick response induced by smilaxin B administered i.c.v. However, naloxone (2 µg), baclofen (10 ng), or CNQX (6-cyano-7-nitroquinoxaline-2,3-dione, 0.5 µg) injected i.c.v. did not affect inhibition of the tail-flick response induced by smilaxin B administered i.c.v. The intrathecal (i.t.) injection of yohimbine (20 µg), but not methysergide (20 µg) and naloxone (2 µg), significantly attenuated inhibition of the tail-flick response induced by smilaxin B administered i.c.v. Our results suggest that GABA_A or NMDA receptors but not opioid, GABA_B, and non-NMDA receptors located at the supraspinal level may play important roles in the production of antinociception induced by smilaxin B administered supraspinally. Furthermore, smilaxin B administered supraspinally may produce its antinociception by activating descending noradrenergic- but not opioidergic- and serotonergic-neurons.

Key words

Smilaxin B - Smilax sieboldii Miq. - Liliaceae - antinociception - CCK - glutamate - GABA - opioid - descending pain control