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The positron emission tomography probes 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG) and 2- tert -butyl-4-chloro-5-{6-[2-(2-[ 18 F]fluoroethoxy)-ethoxy]-pyridin-3-ylmethoxy}-2H-pyridazin-3-one ([ 18 F]BCPP-EF) are designed to evaluate glycolysis and oxidative phosphorylation, respectively, and are both used to estimate neuronal activity. However, previous studies have shown a discrepancy in these probes’ accumulation in the compromised region, possibly due to the presence of activated microglia acting like deleterious or neuroprotective phenotypes. Hence, we evaluated lipopolysaccharide (LPS)- and interleukin 4 (IL4)-stimulated microglial uptake of [ 14 C]2DG and [ 18 F]BCPP-EF to give a new insight into the hypothesis that different uptake of [ 18 F]FDG and [ 18 F]BCPP-EF can be ascribed to the different metabolic pathways activated during microglial activation. LPS or IL4 stimulation increased the proinflammatory or anti-inflammatory marker gene expression in microglial cells. In LPS-stimulated cells, [ 14 C]2DG uptake and glycolysis related gene expression were elevated, and [ 18 F]BCPP-EF uptake was reduced. In IL4-stimulated cells, [ 18 F]BCPP-EF uptake was increased, and [ 14 C]2DG uptake was decreased. The expression of genes involved in glycolysis and mitochondrial complex I subunits was not changed by IL4 stimulation. The uptake of [ 14 C]2DG and [ 18 F]BCPP-EF differs in LPS- and IL4-stimulated polarized microglial cells. The present results suggest that the in vivo accumulation of metabolic tracers [ 18 F]FDG and [ 18 F]BCPP-EF can be influenced by the different aspects of neuroinflammation.

Differences in in vitro microglial accumulation of the energy metabolism tracers [18F]FDG and [18F]BCPP-EF during LPS- and IL4 stimulation