MK4MDD

Study Report

Reference
CitationBrunswick, 2003 PubMed
Full InfoBrunswick, D.J., Amsterdam, J.D., Mozley, P.D. and Newberg, A. (2003) Greater availability of brain dopamine transporters in major depression shown by [99m Tc]TRODAT-1 SPECT imaging. Am J Psychiatry, 160, 1836-1841.

Study
Hypothesis or Background Studies of laboratory animals have shown that administration of antidepressants of all pharmacological classes produces changes in dopamine transporter binding affinity. These observations suggest that dopamine transporter function may play a critical role in the pathophysiology of depression. The present study was an examination of the availability of brain dopamine transporter sites in patients with major depression and in healthy comparison subjects.
Sample Information15 drug-free depressed patients and 46 age- and gender-matched healthy comparison subjects. Patients were required to have taken no antidepressants for at least 7 days, no MAOIs for at least 2 weeks, and no fluoxetine for at least 3 weeks
Method DetailSingle photon emission computed tomographic (SPECT) brain scans were acquired for 15 drug-free depressed patients and 46 age- and gender-matched healthy comparison subjects by using [(99m)Tc]TRODAT-1, a selective dopamine transporter imaging agent. Specific regions of interest in the basal ganglia and supratentorial areas of the brain were examined. Specific uptake values of dopamine transporter [(99m)Tc]TRODAT-1 binding affinity were calculated from the SPECT scan data, and the values for the patients and healthy subjects were compared.
Method Keywordssingle photon emission computed tomography (SPECT)
ResultThe specific uptake values of [(99m)Tc]TRODAT-1 binding were significantly higher in the right anterior putamen (23%), right posterior putamen (36%), left posterior putamen (18%), and left caudate nucleus (12%) of the patients than in the comparison subjects. These differences persisted when the data were further analyzed according to gender and age.
ConclusionsDopamine transporter affinity may be higher than normal in the basal ganglia of depressed patients. These findings suggest that dopamine function may be altered in depression and may also be a mechanism of antidepressant activity.

Relationships reported by Brunswick, 2003