• Masayoshi Tsuruoka, Kiyo Matsutani, and Tomio Inoue.
• Department of Physiology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan. masa@dent.showa-u.ac.jp
• Pain. 2003 Jul 1;104(1-2):353-61.

AbstractBehavioral and neurochemical studies have shown that the coeruleospinal modulation system is activated by peripheral inflammation, and that this modulation system is active in only the dorsal horn ipsilateral, but not in the dorsal horn contralateral, to the site of inflammation; the present study was designed to confirm electrophysiologically this previous finding. Extracellular recordings from dorsal horn neurons were continued for at least 4 h after the induction of inflammation. Unilateral hindpaw inflammation was produced by a subcutaneous injection of carrageenan (2 mg in 0.15 ml saline). Background activity and responses to noxious heating were compared between rats receiving bilateral lesions in the locus coeruleus/subcoeruleus (LC/SC) and non-operated control rats. In neurons located in the dorsal horn ipsilateral to the inflamed paw, prior to inflammation, there was no significant difference in either the background activity or the heat-evoked response in neurons in LC/SC-lesioned compared to LC/SC-intact rats. Four hours after the induction of inflammation, there was a significant increase in both the background activity and heat-evoked response in neurons in LC/SC-lesioned compared to LC/SC-intact rats. In neurons located in the dorsal horn contralateral to the inflamed paw, 4 h after inflammation, no significant increase in either the background activity or the heat-evoked response in neurons in LC/SC-lesioned rats was observed, as well as in the case before inflammation. These results suggest that the coeruleospinal modulation system is active in only the dorsal horn ipsilateral, but not in the dorsal horn contralateral, to the site of inflammation during the development of unilateral hindpaw inflammation.

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