Electroconvulsive Therapy-Induced Prolactin Release as an Epiphenomenon

Electroconvulsive therapy (ECT)-induced prolactin release has been described by many investigators with the expectation that it reflects brain chemistry and thereby the neurochemical pathology of depression or the therapeutic impact of the ECT seizure, analogous to a blood drug level. Neuroendocrine evidence is reviewed to construct plausible mechanisms for ECT-induced prolactin release dependent on three sequential steps outside the brain: posterior pituitary change, transport to anterior pituitary, and prolactin release from anterior pituitary. These mechanisms also explain the prolactin elevations induced by suckling and by estradiol exposure. One mechanism posits seizure-induced interruption of the dopamine flux from posterior to anterior pituitary and consequent decrease of tonic inhibition on prolactin release. The other mechanism depends on a short-chain peptide prolactin-releasing factor. The substantial likelihood of strong posterior pituitary control of ECT-induced prolactin release suggests that it reflects brain chemistry only dimly.