Abstract：
: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.
journal_name
Brain Resjournal_title
Brain researchauthors
Watkins LR,Wiertelak EP,Furness LE,Maier SFdoi
10.1016/0006-8993(94)91948-8subject
Has Abstractpub_date
1994-11-21 00:00:00pages
17-24issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(94)91948-8journal_volume
664pub_type
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