Article Figures & Data
Figures
- Figure 1.
Ten days of IH disrupts Barnes maze performance in WT mice. A, During the probe trial, the distance traveled to initially enter the exit zone was shorter in control mice compared with WT IH10 mice. B, Latency to initial entry was also shorter in control mice. C, Heat maps of the mean entry probability across all false exits (1–19) and Exit 20 during probe trial for the control and WT IH10 mice. D, Comparison of entry probability into the exit zone during the probe trial reveals that control mice had a greater probability of entering the exit zone when compared with WT IH10 mice. (Adapted from Figure 1 in Arias-Cavieres et al., 2020.)
- Figure 2.
Ten days of IH does not affect Barnes maze performance in HIF1a+/− mice. A, In HIF1a+/− mice, the distance initial to initial entry into the exit zone (Exit 20) was similar between 0-HIF1a+/− and 10-HIF1a+/− mice. B, Latency to initial entry into the exit zone (Exit 20) during the probe trial was similar between 0-HIF1a+/− and 10-HIF1a+/− mice. C, Heat maps of the mean entry probability into all zones during the probe trial for 0-HIF1a+/− and 10-HIF1a+/− mice. Entry probability was similar between 0-HIF1a+/− and 10-HIF1a+/− mice; *p < 0.05, **p < 0.01; N.S., not significant. (Adapted from Figure 1 in Arias-Cavieres et al., 2020.)
- Figure 3.
IH suppresses NMDAr-dependent synaptic potentiation in WT hippocampal slices, but NMDAr-dependent LTP is unaffected by IH in the hippocampal slices from HIF1a+/− mice. A, LTPTBS is readily evoked in control (light blue) and is completely blocked by AP5 (light green). B, LTPTBS is present following IH (pink). C, Post hoc comparison of LTPTBS magnitude (60 min following TBS) show significant effects of AP5 or IH10 compared with the control condition. D, LTPTBS was evoked in 0-HIF1a+/− (light gray), 10-HIF1a+/− (light yellow), and 10-HIF1a+/− + AP5 (light green) groups. No difference was found when comparing LTPTBS magnitude of 0-HIF1a+/− and 10-HIF1a+/− mice. Representative traces illustrate baseline (black) and 60 min following HFS (colored trace). Scale bars: 0.2 mV/10 ms. In experiments using AP5, electrophysiological recordings began at 20 min before eliciting LTP (i.e., t = −20), while AP5 was applied 10 min before eliciting LTP (i.e., t = −10). For all experiments, the arrow represents the electric protocol (TBS); ***p < 0.01; N.S., p > 0.05. (Adapted from Figure 2 in Arias-Cavieres et al., 2020.)
- Figure 4.
Effects of IH on NOX4 expression and mitigation of IH-dependent effects on GluN1 expression and Barnes maze performance deficits by antioxidant treatment. A, Comparison of the prooxidant enzyme NOX4 expression levels in hippocampal homogenates from control, WT IH10, 0-HIF1a+/−, and 10-HIF1a+/− mice reveals that NOX4 is increased in WT IH10 but not elevated in either 0-HIF1a+/− or 10-HIF1a+/− mice. B, Normalized GluN1 protein expression was examined in control, WT IH10, IHSaline, and IHMnTMPyP mice. No difference in GluN1 expression was evident between IH10 (open black circles in IH10 label) and IHSaline (open blue circles in IH10 label); therefore, the two groups were merged into the IH10 label for comparisons to control. Comparisons revealed that GluN1 was reduced only in IH10 mice and unchanged in IHMnTMPyP mice. C, Heat maps of the mean entry probability across all false exits (1–19) and the exit zone (Exit 20) during the probe trial for IHSaline and IHMnTMPyP treatments. D, Comparison of entry probability into the exit zone during the probe trial reveals that IHMnTMPyP mice had a greater probability of entering the exit zone when compared with IHSaline mice; *p < 0.05, **p < 0.01, ***p < 0.001; N.S., p > 0.05. (Adapted from Figures 4 and 5 in Arias-Cavieres et al., 2020.)
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