Abstract
Menthol, after topical application, causes a feeling of coolness due to stimulation of ‘cold’ receptors by inhibiting Ca ++ currents of neuronal membranes. Since Ca ++ channel blockers are endowed with analgesic properties, the aim of the present study was to investigate the potential antinociceptive effect of menthol. (−)-Menthol produced a dose-dependent increase in the pain threshold in the mouse hot-plate (3–10 mg kg −1 p.o.) and abdominal constriction (3–10 mg kg −1 p.o.; 10 μg per mouse intracerebroventricularly (i.c.v.)) tests. The antinociceptive effect of (−)-menthol was antagonised by the unselective opioid antagonist naloxone and by the selective κ-antagonist nor-NBI. Conversely, CTOP (μ-antagonist), 7-benzylidenenal-trexone (δ 1 antagonist) and naltriben (δ 2 antagonist) did not prevent (−)-menthol antinociception. In both tests, (+)-menthol (10–50 mg kg −1 p.o.; 10–30 μg per mouse i.c.v.) was unable to modify the pain threshold. These results indicate that (−)-menthol is endowed with analgesic properties mediated through a selective activation of κ-opioid receptors.
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