Behavioral and neuroendocrine effects of low dose ET-495: Antagonism by haloperidol

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Abstract
Low doses of the dopamine agonist ET-495 were administered to non-psychotic 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.