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Minami, T. et al.

Functional evidence for interaction between prostaglandin EP3 and kappa-opioid receptor pathways in tactile pain induced by human immunodeficiency virus type-1 (HIV-1) glycoprotein gp120.

HIV-1 glycoprotein gp120 administered intrathecally induces tactile pain (allodynia) in animals. In the present study, we investigated the mechanism of gp120-induced allodynia and possible functional connections with factors modulating pain transmission at the spinal level. Gp120 evoked allodynia in a dose-dependent manner with the maximum effect at 1 pg/mouse, and stimulated a rapid increase in intracellular free Ca2+ concentration ([Ca2+]i) in the dorsal horn cells of the spinal cord. These responses evoked by gp120 were blocked by galactocerebroside. The gp120-induced allodynia was also attenuated by the non-steroidal anti-inflammatory drug indomethacin, which inhibits prostaglandin synthesis, and did not develop in mice lacking the EP3 prostaglandin E receptor subtype ( EP3(-/-)). Pretreatment of spinal slices with indomethacin dose-dependently decreased the percentage of the cells that showed increased [Ca2+]i in response to gp120, and the decrease was reversed by addition of the selective EP3 agonist ONO-AE-248. The kappa-opioid agonist U-50,488 significantly enhanced the gp120-stimulated increase in [Ca2+]i in spinal slices prepared from EP3(-/-) mice, and the simultaneous addition of U-50,488 with gp120 reproduced the gp120-induced allodynia in EP3(-/-) mice. These results suggest that gp120 induced allodynia by increasing [Ca2+]i, concomitant with activation of prostanoid EP3 and kappa-opioid receptors in the spinal cord.[1]

References

Functional evidence for interaction between prostaglandin EP3 and kappa-opioid receptor pathways in tactile pain induced by human immunodeficiency virus type-1 (HIV-1) glycoprotein gp120. Minami, T., Matsumura, S., Mabuchi, T., Kobayashi, T., Sugimoto, Y., Ushikubi, F., Ichikawa, A., Narumiya, S., Ito, S. Neuropharmacology (2003) [Pubmed]

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