Many evidences stress the implication of dopamine systems in the pathophysiology of depression. Currently, few and uncertain results are available on pre-synaptic dopaminergic dysfunction during depression. Our aim was to assess dopamine transporter (DAT) density in Major Depressive Disorder (MDD) with marked psychomotor retardation or anhedonia using 123I-FP-CIT SPET.

15 drug-free patients (F/M=8/7, mean age=44.6 SD=12.6 years) with MDD according to DSM-IV-R criteria, were enrolled for:

1. 1. Psychometric assessment (of depression, anxiety, anhedonia and psychomotor impairment using Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, Snaith-Hamilton Pleasure Scale and Depression Retardation Rating Scale);

2. 2. DAT measurement with 123I-FP-CIT SPET.

14 healthy subjects, comparable for gender and age, formed the control group.

Patients had moderate-to-severe depression. They showed a significant decrease in DAT density in whole striatum bilaterally compared to controls. Furthermore, mean 123I-FP-CIT uptake ratios were significantly lower in caudate and putamen bilaterally. Patients were then divided into two subgroups: 7 had a relevant psychomotor retardation without anhedonia; 8 had severe anhedonia without retardation. The psychomotor retardation group showed significantly lower 123I-FP-CIT uptake ratios in left putamen compared to the anhedonic group. An inverse correlation between DAT density in left putamen and retardation scores were observed.

Present results confirm a decrease of DAT binding in MDD. Low DAT availability could represent a compensatory mechanism following dopamine reduction. Moreover, DAT reduction seems to be related more to retardation than anhedonic features, in agreement with previous PET imaging findings.