6-cyano-7-nitroquinoxaline-2-3-dione and Disease

The spinal cord dorsal horn contains neural mechanisms which can greatly facilitate pain. We have recently shown that 'illness'-inducing agents, such as intraperitoneally administered lipopolysaccharide (LPS; bacterial endotoxin), can produce prolonged hyperalgesia. This hyperalgesic state is mediated at the level of the spinal cord via activation of the NMDA-nitric oxide cascade. However, prolonged neuronal depolarization is required before such a cascade can occur. The present series of experiments were aimed at identifying spinal neurotransmitters which might be responsible for creating such a depolarized state. These studies show that LPS hyperalgesia is mediated at the level of the spinal cord by substance P, cholecystokinin and excitatory amino acids acting at non-NMDA sites. No apparent role for serotonin or kappa opiate receptors was found.

Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Animals; Biphenyl Compounds; Cholecystokinin; Disease; Excitatory Amino Acids; Hyperalgesia; Injections, Spinal; Lipopolysaccharides; Neuropeptides; Rats; Rats, Sprague-Dawley; Receptors, Opioid, kappa; Serotonin; Spinal Cord; Substance P