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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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6-Cyano-7-nitroquinoxaline-2,3-dione / pharmacology
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Animals
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Biphenyl Compounds / pharmacology
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Cholecystokinin / antagonists & inhibitors
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Cholecystokinin / pharmacology
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Disease
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Excitatory Amino Acids / physiology*
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Hyperalgesia / etiology*
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Hyperalgesia / physiopathology
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Hyperalgesia / prevention & control
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Injections, Spinal
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Lipopolysaccharides / antagonists & inhibitors
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Neuropeptides / physiology*
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Rats
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Rats, Sprague-Dawley
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Receptors, Opioid, kappa / antagonists & inhibitors
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Serotonin / pharmacology
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Spinal Cord / chemistry*
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Substance P / antagonists & inhibitors
Substances
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Biphenyl Compounds
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Excitatory Amino Acids
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Lipopolysaccharides
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Neuropeptides
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Receptors, Opioid, kappa
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Serotonin
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Substance P
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6-Cyano-7-nitroquinoxaline-2,3-dione
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Cholecystokinin
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CP 96345