Investigations of the possible role for carbon monoxide (CO) in thermal and mechanical hyperalgesia in the rat

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Abstract
Although recent reports have shown that production of nitric oxide (NO) is primarily involved in thermal hyperalgesia, the available behavioral evidence suggests that the signal transduction mechanisms involved in mechanical hyperalgesia, in general, do not involve NO. We report here that production of another labile gaseous messenger, carbon monoxide (CO) appears to be involved in mechanical but not thermal hyperalgesia produced in models of acute (intrathecal administration of glutamate receptor agonists) and persistent (intraplantar injection of zymosan) hyperalgesia. Together with results of previous studies, these results are consistent with a primary role for NMDA receptors and NO in thermal hyperalgesia and an involvement of AMPA and metabotropic glutamate receptors and CO in mechanical hyperalgesia.

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