Discussion Intrathecal administration of GABA receptor antagonists has been shown to cause hyperalgesia and allodynia. Constitutively, increasing endogenous GABA activity in the spinal cord relieves pain resulting from noxious and harmless mechanical and thermal stimuli. Different GABA receptors have different roles in relieving thermal and mechanical pain in different animal pain models. To date, there is no study that has examined the involvement of GABA A and GABA B in the sensory dimension of neuropathic pain resulting from spinal cord compression. The present study tests the hypothesis that GABA A or GABA B receptors contribute to the allodynia and hyperalgesia observed after spinal cord injury. The results showed that the effect of GABA A and GABA B receptors on mechanical hyperalgesia is similar but these receptors have different effects on thermal hyperalgesia. Although the use of baclofen as a GABA B receptor agonist does not affect thermal pain, thermal hyperalgesia resulting from spinal cord injury was significantly alleviated by several doses of the GABA A agonist, muscimol. Both baclofen and muscimol are able to reduce the mechanical and cold allodynia observed after spinal cord injury, but the effect of baclofen is dose-dependent and has no effect at the higher doses used in this study. Although almost all doses of muscimol were used in this study, the amount of cold and mechanical allodynia were reduced. The other result obtained in this study is the short-term effect of the GABA agonist. The anitinociceptive effect of baclofen and muscimol appears to be maximal 15 minutes after injection and gradually decreases over time, and their analgesic effect disappears 3 hours after injection. Currently, pharmacological mechanisms influence the neuro...... half of the article ..... .tive to intrathecal administration of morphine compared to tactile allodynia. Therefore, examining both modalities is important when examining the spinal pharmacology of the nerve injury state. Our results provide the first demonstration that GABAA but not selective GABA B receptor agonists reverse the thermal hyperalgesia produced by spinal cord injury. In parallel, we demonstrate that in spinal cord lesions similar to peripheral nerve lesions, GABAA and GABAB receptor agonists reduce cold and tactile allodynia and mechanical hyperalgesia. Furthermore, our studies used a sensitive and reproducible test of motor function to compare the antiallodynic, antihyperalgesic, and motor effects of GABA receptor agonists. Data suggest that GABAA agonists may be effective in treating neuropathic pain with thermal hyperalgesia without sensory or motor side effects.