Behavioral and neuroendocrine effects of low dose ET-495: antagonism by haloperidol.
Low doses of the dopamine agonist ET-495 were administered to nonpsychotic volunteer subjects by slow intravenous infusion, followed by a bolus of 1.5--2.5 mg haloperidol. ET-495 caused progressive dysphoria and sedation (in some cases, light sleep), effects believed to be mediated by dopaminergic inhibition. However, ET-495 also elevated growth hormone and suppressed prolactin, typical responses to dopamine agonist activity. Haloperidol reversed both the sedation and prolactin suppression induced by ET-495. These findings suggest: (1) that the sedation and hormonal responses were produced by stimulation of dopamine receptors; (2) that neurotransmitter systems mediating behavioral and neuroendocrine regulation may have differential neuropharmacological characteristics.
D000328:Adult; D004305:Dose-Response Relationship, Drug; D013006:Growth Hormone / Q000097:blood*; D006220:Haloperidol / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009325:Nausea / Q000188:drug therapy; D010879:Piperazines / Q000494:pharmacology*; D010891:Piribedil / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011388:Prolactin / Q000097:blood*; D011595:Psychomotor Agitation / Q000188:drug therapy; D012894:Sleep Stages / Q000187:drug effects*
D010879:Piperazines; D011388:Prolactin; D013006:Growth Hormone; D010891:Piribedil; D006220:Haloperidol