286. Effects of depression on psychomotor and neuromotor slowing

Studiesinvestigatingthe biologicalbasis of seasonalaffectivedisorder (SAD)and the mechanismsof actionof light therapyhavefocussedon serotonergicmechanisms.Sofar, the potentialrole of catecholaminergic pathwayshas not been fully explored.We comparedthe effects of tryptophandepletionwiththoseof catecholaminedepletionin a doubleblind, placebo-controlled, balanced, rsndomired crossover study. Patients with SADwhohad respondedto a standardizedregimenof daily 10,OOO-IUX light treatment were included.Tryptopharrdepletionwas induced by ingestion of aminoacidcapsules and a tryptophsn-free sminoacidbeverage,catecholaminedepletionbyingestionofthetyrosine hydroxylaseinhibitor alpha-methyl-para-tyrosine (AMPT).Diphenhydrarnineanda shambeveragewereusedin the placebocondition.Main effectsofconditionandtime,andtheinteractionofconditionx timewere assessedusing 2-wayanalysesof variancewith repeatedmeasures.Of the 16patientsenrolled,3didnotcompletethe study,andtheirdatawere not used for statistical purposes.As predicted, tryptophsndepletion significantlyreducedplasma total and frm tryptophsmconcentrations, catechokurtinedepletion significantlyreduced plasma 3-methoxy-4hydroxyphenylethylenglycol and homovsnillicacid levels.Bothtryptophsmdepletionand catecholaminedepletion,comparedto shamdepletion, induced a transient reoccurrence of depressive symptoms as measuredwith the HamiltonDepressionRatingScale, SeasonalAffective DisorderVersion.The antidepressanteffects oflight therapywere dismptedby both tryptophandepletionand catechokuninedepletion. These tindingssuggestthat brain serotoninand catecholaminesystems maybe involvedin the mechanismof actionof lighttherapy.