Naloxone fails to block ECT-induced prolactin increase

Abstract

The rapid, but transient, prolactin (PRL) induring the electroconvulsive therapy (ECT) is well known (Ohman et al. 1976; Skrabanek et al. 1981; Papakostas et al. 1984), although the underlying mechanism mediating this effect remains speculative. It has been suggested that endogenous opioid peptides may be involved (Skrabanek et al. 1981; Deakin et al. 1983): these substances, among other effects, increase PRL in man, and this increase can be blocked by small doses of naloxone (Grossman and Rees 1983; Morley 1983). The question then arises whether or not the ECT-induced PRL increase is mediated via stimulation of opioid secretion. In this study, the role of opioids in the ECTinduced prolaetin increase was tested by the administration of the opioid receptor antagonist, naloxone, to five female melancholic patients who were undergoing treatment with ECT. The patients' ages ranged between 38 and 63 years. With the exception of low doses of benzodiazepines (flunitrazepam) given at bed time, they were free from psychotropics or any other drugs