Calcitonin reverts pertussis toxin blockade of the opioid analgesia in mice

The aim of this paper is to study the influence of salmon calcitonin (SCT) on opioid analgesia when opioid transduction pathways are functionally uncoupled from G i/o proteins by treatment with pertussis toxin (PTX). The antinociceptive effect of morphine and three selective opioid agonists, [D–Ala 2,N–Me–Phe 2,Gly 5–ol]enkephalin (DAMGO) (OP 3-μ receptor agonist), [D–Pen 2,5]-enkephalin (OP 1-δ receptor agonist) and trans-(±)-3,4-dichloro- N-methyl-N-[2–1(–pyrrolidinyl)cyclohexyl]-benzene-acetamide methane sulfonate (U-50, 488H) (OP 1-κreceptor agonist) was evaluated, using the tail flick test, in mice treated with PTX or with PTX and SCT. PTX blocked the antinociceptive effect of the opioids, being the antinociception similar in control animals and in mice treated with PTX and SCT. Thus, SCT prevents the effect of the blockade of G i/o-proteins. From this it could be suggested that calcitonin activates alternative antinociceptive mechanisms that are not dependent on G i/o-proteins.