Presynaptic dopamine function in striatum of neuroleptic-naive schizophrenic patients

Hietala, Jarmo
Syvalahti, Erkka
Vuorio, Klaus
Rakkolainen, Viljo
Bergman, Jorgen
Haaparanta, Merja
Solin, Olof
Kuoppamaki, Mikko
Kirvela, Olli
Ruotsalainen, Ulla
Salokangas, Raimo K R

Department of Pharmacology, University of Turku, 20520 Turku, Finland (J Hietala MD, E Syvalahti MD, M Kuoppamaki MD); Turku Medical Cyclotron/PET Project (J Hietala, E Syvalahti, M Haaparanta MSc, M Kuoppamaki, U Ruotsalainen MSc); Turku City Psychiatric Hospital (K Vuorio MD, V Rakkolainen MD); Accelerator Laboratory, Abo Akademi University (J Bergman MSc, O Solin PhD); Department of Anaesthesiology, Turku University Hospital (O Kirvela MD); and Department of Psychiatry, Turku University Hospital (Prof R K R Salokangas MD)
Correspondence to: Dr Jarmo Hietala
This study was financially supported by the Jalmari and Rauha Ahokas Foundation. We thank Vesa Oikonen and Esa Eronen and staffs in the Turku PET laboratory, Turku City Psychiatric Hospital, and MRI unit, Department of Radiology, Turku University Hospital.

The Lancet 346(8983):p 1130-1131, October 28, 1995.

Presynaptic dopamine function (6-[(¹⁸) F]-fluorodopa uptake) in the brains of seven neuroleptic-naive first-admission schizophrenic patients and eight healthy controls was studied with positron emission tomography. The fluorodopa influx constant (K_i ) in putamen was higher in the patients than in controls (average mean: 0.0149 vs 0.0129, p=0.034). The changes in caudate were smaller but significantly lateralised to the left caudate. There was one catatonic schizophrenic patient in our sample. This patient had lower striatal K_i than any control. Alterations in striatal presynaptic dopamine function may constitute a part of disrupted neural circuits that predispose to schizophrenic psychosis.

Lancet 1995; 346

1130-31