Neuroendocrine study of the mechanism of action of electroconvulsive therapy.
The authors' earlier studies indicated that prolactin (PRL) response to electroconvulsive therapy (ECT) was not the result of stress reaction, because the secretion of other stress-sensitive hormones showed no parallel increase. The results of the present investigation are consistent with this findings as diazepam pretreatment failed to influence the PRL response induced by ECT. The rise of the serum PRL level was accompanied by a slight but significant decrease of the serum dopamine-beta-hydroxylase activity. A significant negative correlation was found between baseline serum dopamine-beta-hydroxylase activity and PRL response. These data indicate a correlation between serum dopamine-beta-hydroxylase activity and central dopaminergic function. PRL response to ECT is supposed to be the result of the dopaminergic action of ECT.
D000328:Adult; D003975:Diazepam; D004299:Dopamine beta-Hydroxylase / Q000097:blood*; D004565:Electroconvulsive Therapy; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008875:Middle Aged; D011388:Prolactin / Q000097:blood*; D012559:Schizophrenia / Q000097:blood / Q000628:therapy*
D011388:Prolactin; D004299:Dopamine beta-Hydroxylase; D003975:Diazepam; D006854:Hydrocortisone