ABSTRACT. The tumoral uptake of fluorine-18-deoxyglucose (FDG) is based upon enhanced glycolysis. Following injection, FDG is phosphorylated and trapped intracellularly. An important mechanism to transport FDG into the transformed cell is based upon the action of glucose transporter proteins; furthermore, highly active hexokinase bound to tumor mitochondria helps to trap FDG into the cell. In addition, enhanced FDG uptake may be due to relative hypoxia in tumor masses, which activates the anaerobic glycolytic pathway. In spite of these processes, FDG uptake is relatively aspecific since all living cells need glucose. Clinical use is therefore recommended in carefully selected patients. NUCL MED BIOL 25;4:317-322, 1998.

Results suggest that cortical D(2) dopamine receptors are a common target of traditional and atypical antipsychotics for therapeutic action. Higher in vivo binding to the D(2) receptors in the cortex than in the basal ganglia is suggested as an indicator of favourable profile for a putative antipsychotic compound.