Abstract
Plasma prolactin (PRL) levels rise sharply in response to spontaneous or electrically induced seizures and although the relationship between this neuroendocrine response and the clinical effects of electmconvulsive therapy (ECT) has yet to be demonstrated, the possibility that studying this phenomenon may shed some light on the mechanism of action of ECI remains (Fink 1979, Abrams 1988). The ECTinduced PRL release is markedly reduced followir/; pretreatment with the ergot derivative m.'thysergide, a serotonin (5-HT) receptor an, ~gonist (Papakostas et al 1988, Zis et al 1989a). i lowever, the hypothesized role of 5-HT in this neuroendocrine response remains uncertain for several reasons. First, the use of ergot derivatives as 5-HT receptor antagonists to study the regulation of PRL release has been criticized on the grounds that PRL secretion is tonically inhibited by dopamine, and these compounds pessess dopamine receptor agonist properties (Lambert~ and MacLeod 1979). Second, i¢ has been shown that pretreatment with the 5-HT2 antagortist ketanseri'n and ritanserin fails to attenuate the ECT-induced PRL surge (Zis et al 1989b, Papakostas et al 1990). And third, it was re-
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