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. Author manuscript; available in PMC: 2020 Apr 9.
Published in final edited form as: Physiol Behav. 2019 Feb 21;204:140–150. doi: 10.1016/j.physbeh.2019.02.025

Fig. 5.

Fig. 5.

Fourth ventricle 2DG evokes a counter-regulatory hyperglycemia that is suppressed by FC and adenosine antagonists. Maximal percent change in blood glucose levels relative to baseline levels were averaged within each group. Maximal peak responses for the 2DG (alone) group averaged 36.0 ± 7.4%change. While 4 V application of vehicle controls (saline or 1:4 DMSO/saline) or FC (alone) or caffeine (alone; data not shown here) had no effect on glucose levels, pretreatment of the 4 V with FC blocked the effect of subsequent 2DG to increase blood glucose (FC + 2DG: 3.1 ± 2.0%). Similarly, pretreatment with caffeine or DPCPX suppressed the glycemic effects of 2DG (caffeine+2DG = 5.7 ± 2.8%; DPCPX+2DG = 11.1 ± 2.4%). In contrast, the NMDA antagonist, MK801, did not block the 2DG effect to increase blood glucose (MK801 + 2DG = 22.2 ± 6.4%). One way ANOVA F7,38 = 9.78, p < .0001; Dunnett’s post-hoc test * p < .05. These results are consistent with a counter-regulatory hyperglycemia triggered by astrocytes utilizing adenosine as a gliotransmitter. (Adapted from Rogers et al., 2016, Am J Physiol Regul Integr Comp Physiol 310: R1102–R1108).