Abnormal activity of polymodal receptors induced by clioquinol (5-chloro-7-iodo-8-hydroxyquinoline).

To know possible involvement of primary afferents in paresthesia of subacute myelo-optico-neuropathy (SMON), influence on polymodal receptor, a type of nociceptor, of its causal agent clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) was tested using in vitro testis-superior spermatic nerve preparations of dogs. Exposure to clioquinol (greater than 1 microM) induced an abnormal bursting activity in polymodal receptors, and thereafter the receptors were sensitized to an algesic stimulus (hypertonic saline) and gained a new sensitivity to cold, while pure mechanoreceptors were not influenced. On the other hand, clioquinol glucuronide (100 microM), a detoxicated form, had no such effects. These results are consistent with several clinical observations of sensory aberrations, suggesting possible involvement of the abnormal activities of polymodal receptors in SMON paresthesia.