Neuroendocrine evidence for increased responsiveness of dopamine receptors in humans following electroconvulsive therapy.
The previous finding that electroconvulsive therapy (ECT) enhances effects of dopamine (DA) agonists was further investigated in the present clinical experiment using neuroendocrine techniques. Apomorphine chloride (AP) (0.18-0.24 mg IV) induced stimulation of growth hormone (GH) and suppression of prolactin (PRL), as shown 2-3 days before and after ECT in mentally depressed patients (N = 12) and therapy-resistant parkinsonian patients with on-off phenomena (N = 9). AP-stimulated GH secretion was not significantly affected by ECT, whereas AP-induced suppression of PRL, expressed as percentage of baseline PRL levels, was significantly enhanced after ECT. Changes in clinical and hormonal parameters were not significantly correlated. Control patients not receiving ECT showed no significant changes in AP-induced GH secretion or PRL suppression in repeated investigations. The results support the view that ECT increases responsiveness of DA receptors and indicates that AP-induced suppression of PRL is a useful model to reflect these changes in humans.
D000328:Adult; D000368:Aged; D001058:Apomorphine / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology; D003866:Depressive Disorder / Q000097:blood / Q000628:therapy*; D004565:Electroconvulsive Therapy; D005260:Female; D013006:Growth Hormone / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010302:Parkinson Disease, Secondary / Q000097:blood / Q000628:therapy; D011388:Prolactin / Q000097:blood*; D011954:Receptors, Dopamine / Q000494:pharmacology*; D012110:Reserpine / Q000494:pharmacology
D011954:Receptors, Dopamine; D012110:Reserpine; D011388:Prolactin; D013006:Growth Hormone; D003000:Clonidine; D001058:Apomorphine