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. 2020 Jul 15;40(29):5681–5696. doi: 10.1523/JNEUROSCI.2876-19.2020

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Copyright © 2020 Kealy, Murray et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License Creative Commons Attribution 4.0 International, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 3. — Low blood glucose concentration drives LPS-induced hypoactivity. A, Linear regression analyses of locomotor activity (squares crossed/3 min) versus blood glucose concentration (mmol/l) in animals challenged with saline (n = 14) and LPS (n = 17). Blood glucose concentrations significantly correlated with locomotor activity in LPS-treated mice. B, LPS significantly reduces spontaneous activity in the open field compared with saline-treated controls. Prompting inactive mice to move by gently nudging them with a fingertip results in similar levels of activity, showing that LPS mice are capable of moving but are not motivated to do so. C, Timeline for treatments and sampling times. Glucose (2 g/kg, i.p.) was administered 1.5 h post-LPS challenge (250 µg/kg, i.p.), and open field behavior was measured 2 h post-LPS challenge. Five minutes after open field testing, mice were euthanized, CSF samples taken, blood glucose levels assessed, and plasma collected for IL-1β ELISA. In one group, 2-DG (2 g/kg, i.p.) was given 3 h before LPS. D, LPS (250 μg/kg, i.p.; n = 8) induced IL-1β production (F_(1,25) = 29.88; p < 0.001), which was unaffected by glucose co-administration (n = 7; 90 min post-LPS) but blocked by 2-DG administration (intraperitoneal, n = 5, #p = 0.0296 vs LPS+saline). E, Locomotor activity was suppressed by LPS (main effect of LPS: F_(1,27) = 13.39; p = 0.0011) but rescued by glucose co-administration (interaction between treatments: F_(1,27) = 10.48; p = 0.0032); **significant difference between LPS+glucose (n = 9) and LPS+saline (n = 8), and these were not significantly different to saline+saline (n = 7) or saline+glucose controls (n = 7). 2-DG+LPS completely suppressed locomotor activity in LPS-treated mice (t₍₁₃₎ = 5.766; ###p < 0.0001 vs LPS+saline). F, Blood glucose was suppressed by LPS (main effect: F_(1,27) = 60.00; p < 0.0001) and modestly increased by glucose (main effect: F_(1,27) = 6.721; p = 0.0152), and post hoc tests showed that LPS+glucose was significantly different to LPS+saline. G, Glucose treatment 1.5 h after LPS provided significant but transient protection against LPS-induced hypoglycemia. H, CSF (from the same animals) showed a main effect of LPS (F_(1,22) = 39.85; p < 0.0001) and a strong main effect of glucose (F_(1,22) = 14.57; p = 0.0009). LPS+glucose was significantly different to LPS+saline in post hoc analysis (p < 0.05). Two data points in these analyses represent two pooled samples each (in the saline+glucose and LPS+saline groups where some CSF samples were too low in volume to be assessed). They have been highlighted as slightly larger, filled symbols. I, CSF lactate levels (same animals) were not altered by the treatments described. Again, the same samples were pooled for this analysis. In LPS-naive mice, 2-DG on its own does not significantly affect (J) spontaneous activity nor does it: have any effect on (K) blood glucose. Significance levels for Bonferroni post hoc tests: *p < 0.05, **p < 0.01, ***p < 0.001. All data are expressed as mean ± SEM.