Implications of Ca(2+)-activated Cl(-) channels in the delta-opioid receptor-mediated antinociception in the mouse spinal cord.

Abstract

The present study was designed to investigate the role of Ca(2+)-activated Cl(-) channels in the spinal opioid receptor-mediated antinociception using the mouse tail-flick assay. The antinociception induced by intrathecal (i.t.) administration of a selective delta-opioid receptor agonist [D-Ala(2)]deltorphin II (10 microgram, i.t.) was significantly attenuated by i.t.-pretreatment with selective Ca(2+)-activated Cl(-) channel blockers, IAA-94, flufenamic acid and niflumic acid. By contrast, IAA-94 had no effect on the antinociception induced by i.t.-treated with either the selective mu-opioid receptor agonist [D-Ala(2),N-MePhe(4), Gly-ol(5)]enkephalin or the kappa-opioid receptor agonist U-50,488H. The present results provide evidence for the first time that the Ca(2+)-activated Cl(-) channel is, at least in part, implicated in the delta-, but not the mu- and kappa-opioid receptor-mediated antinociception in the mouse spinal cord.

Cite this paper

@article{Yamazaki2000ImplicationsOC, title={Implications of Ca(2+)-activated Cl(-) channels in the delta-opioid receptor-mediated antinociception in the mouse spinal cord.}, author={Mitsuaki Yamazaki and Hiroyuki Mizoguchi and Masahiko Ohsawa and Leon Fu Tseng and T Suzuki and Mitsuo Narita}, journal={Neuroscience letters}, year={2000}, volume={295 3}, pages={113-5} }