Opiate receptor function may be modulated through an oxidation-reduction mechanism.

Cupric ion, a thiol oxidant, caused naloxone-reversible analgesia when injected intracerebroventricularly in mice; its potency was close to that of morphine. Dithiothreitol, a thiol reductant, reversed the analgesia induced by cupric ion and antagonized analgesia induced by morphine. Oxidized dithiothreitol had no effect. These findings, together with evidence for redox modification of opiate receptor binding in vitro, suggest that a mechanism of oxidation-reduction of thiols may modulate opiate receptor function.