Psychopharmacology

, Volume 144, Issue 3, pp 282–285

Striatal dopamine transporter density in major depression

Authors

  • Teijamari Laasonen-Balk
    • Department of Psychiatry, Kuopio University Hospital, FIN-70210 Kuopio, Finland
  • Jyrki Kuikka
    • Department of Clinical Physiology, Kuopio University Hospital, FIN-70210 Kuopio, Finland
  • Heimo Viinamäki
    • Department of Psychiatry, Kuopio University Hospital, FIN-70210 Kuopio, Finland
  • Minna Husso-Saastamoinen
    • Department of Clinical Physiology, Kuopio University Hospital, FIN-70210 Kuopio, Finland
  • Johannes Lehtonen
    • Department of Psychiatry, Kuopio University Hospital, FIN-70210 Kuopio, Finland
  • Jari Tiihonen
    • Department of Forensic Psychiatry, University of Kuopio, Niuvanniemi Hospital, FIN-70240 Kuopio, Finland
ORIGINAL INVESTIGATION

DOI: 10.1007/s002130051005

Cite this article as:
Laasonen-Balk, T., Kuikka, J., Viinamäki, H. et al. Psychopharmacology (1999) 144: 282. doi:10.1007/s002130051005

Abstract

Rationale: There are no previous data available regarding [123I]β-CIT binding to the dopamine transporter sites in the basal ganglia in depressed patients. Objective: The present study tested the hypothesis that the brain DAT density in depressed patients is lower than that in matched healthy controls. Methods: Fifteen drug-naive outpatients with major depression and 18 healthy controls were investigated using single photon emission computerized tomography (SPECT) with a high-affinity dopamine transporter specific radioligand, 123I-labeled β-CIT (2β-carbomethoxy-3β-(4-iodophenyl)-tropane). Results: We found a significantly higher [123I]β-CIT uptake in both sides of the basal ganglia in patients with major depression than in the controls (Mann-Whitney U-test, P = 0.002 on the right and P = 0.003 on the left). Conclusions: The radioligand uptake reflecting the DAT density was significantly higher among the patients than in the controls. This finding is unexpected, since it is generally believed that monoaminergic neurotransmission is lower in depression, and therefore it could be assumed that a reduction in dopamine transmission would lead to secondary down-regulation of DAT density. However, it is possible that up-regulation of the DAT may be the primary alteration, which leads to lower intrasynaptic dopamine concentration and to lower dopamine neural transmission.

Key words DepressionSPECTβ-CITDopamineTransporter

Copyright information

© Springer-Verlag Berlin Heidelberg 1999