AIM To investigate the relationship between spinal GABA A re ce ptors and spinal
analgesia of ketamine and determine whether
the antinociceptive action of intrathecal ketamine on GABAergic neurons occur presynaptically or po stsynaptically. METHODS Antinociceptive tests in Kunming mice were investigated with tail-immersion test and acetic-induced writhing test. The ef fects of intrathecal (ith) ketamine on the pain threshold and the influence of p retreatment with GABA A receptor antagonist bicuculline (Bic, 0.05, 0.1, 0. 2 μ g), GABA synthesis inhibitor L-allylglycine(AG, 200 mg·kg - 1, ip) and their combination on the pain threshold and spinal
analgesia of ket amine (100 μg) were observed. RESULTS Dose-dependent analgesia was observed following ith ketamine (50, 100 μg) . Bic ith alon e had no effect on the pain threshold. Bic ith (0.1, 0.2 μg) , but not 0.05 μg, significantly inhibited the spinal analgesia of ketamine. AG ip or the combination of AG and Bic (0.05, 0.1 μg, ith) had no effect on the p ain threshold. However, pretreatment with ip AG significantly reduced the spinal analgesia of ketamine. Furthermore, after pretreatment with AG, Bic (0.01 μg, ith) had no inhibitory effect on the spinal analgesia of ketamine. CONCLUS ION
Spinal cord is one of the targets of ketamine analgesia. The spinal a nalgesia of ketamine is partly mediated by spinal GABA A receptors, possibly via a presynaptical mechanism in mice. But the direct action of ketami ne on spinal GABA A receptors may be of little importance to its analgesia.