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. 2015 Oct 7;11(4):561–569. doi: 10.1007/s11302-015-9474-3

Fig. 4.

Fig. 4

Mapping the role of A2BRs on glycogen synthesis and lactate release. In acute 400-μm-thick coronal frontocortical and rostrocaudal striatal slices from C57Bl/6j mice, brain slices were divided into two groups and they were submerged in an assay solution containing the metabolizable glucose analogue, 14C6-glucose (50 nM), at 37 °C under continuous gassing with a mixture of 95 % O2 and 5 % CO2. One chamber with a group of slices from the three brain areas was exposed to MRS1754; the other group was exposed to its vehicle, DMSO (0.1 %, control). After 90-min incubation, the slices were washed three times in ice-cold assay solution, collected in 2 mL NaOH (0.5 M). After dissolving the slices, 200 μL of these samples was used to count total 14C retention in the slices and protein quantities; the rest of the 1800 μL was used to precipitate glycogen and count its 14C content as before [26]. Lactate content in the bath at the end of the 90-min incubation period was assessed with a lactic acid assay kit. Bars represent the mean ± SEM of individual measurements from n = 6–8 mice. *P < 0.05, ***P < 0.001 versus control