Mechanism of the analgesic effect of calcitonin evidence for a twofold effect: morphine-like and cortisone-like

Conclusions

Binding sites (receptors) for Calcitonin have been found in several regions of the Central Nervous System and more especially in the medial basal hypothalamus and in the pituitary. Furthermore, proopiocortine peptides have been identified in the same loci.

This leads us to put forward the following hypothesis:

• 1 By binding with these receptors, Calcitonin induces a proopiocortine secretion resulting in the release of both Beta-Endorphin and ACTH.

• 2 The strong secretion of ACTH may act by reducing the local inflammatory process and consequently the discharge of nociceptive nerve endings.

• 3 Beta-Endorphin induces a high level of activity of the nucleus Raphe Magnus and of the Serotonergic Descending System which, according to the hypothesis of Jessei and Iversen, controls nociceptive afferents by means of presynaptic inhibition of substance P release.

This is in agreement with the results obtained by Clementi et al (1984), who have demonstrated that a serotonergic blocking agent (Methysergide) antagonized the analgesic effect of salmon Calcitonin.