Abstract
One of the most consistently reported immediate effects of electroconvulsive therapy (ECT) is a rapid and transient increase of serum prolactin (PRL) (Ohman et al. 1976; Deakin et al. 1983), but the underlying mechanism mediating this response remains unclear. Interventions such as pretreatment with the alpha-adrenergic receptor blocker phentolamine (Klimes et al. 1978), diazepam (Arato and Bagdy 1982), or the opioid antagonist naloxone (Papakostas et al. 1985) do not seem to affect this ECT-induced PRL secretion. Similarly, omission of anticonvulsive premedication (Klimes et al. 1978), or omission of pretreatment with atropine (Scott et al. 1986), do not influence the PRL response to ECT. On the other hand, it has been suggested that ECT exerts a selective hypothalamic+uitary axis effect and that the secretion of PRL in particular is due to the stimulation of central serotonergic mechanisms (Whalley et al. 1987). In this study, the role of the serotonergic system in the ECT-induced PRL secretion was tested using the serotonin receptor blocking properties of methysergide.
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