Figure 5.

Antioxidant treatment mitigates the IH-dependent effects on GluN1 expression, LTP_TBS, and performance in the Barnes maze. A, left, Representative Western blottings of GluN1 and GAPDH from Control, IH₁₀, wild-type mice treated with saline during 10 d of IH (i.e., vehicle control exposed to IH, IH_Saline, n = 4), wild-type mice treated with MnTMPyP during 10 d of IH (IH_MnTMPyP). Right, Normalized GluN1 protein expression was examined in control (n = 4), IH₁₀ (n = 4), IH_Saline (n = 4), IH_MnTMPyP (n = 4). No difference in GluN1 was evident between IH₁₀ (open black circles in IH₁₀ label) and IH_Saline (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 and unchanged in IH_MnTMPyP. B, In hippocampal slices from IH_MnTMPyP, LTP_TBS (n = 5) could be reliably evoked contrasting the effect of IH₁₀ on LTP_TBS (Fig. 2B). Scale bars: 0.2 mV/10 ms. The arrow represents the TBS protocol. C, The total latency to exit the Barnes maze progressively decreased in both IH_Saline (n = 11, pink lines represent individual performance) and IH_MnTMPyP (n = 10, purple lines represent individual performance), suggesting that both groups could learn the exit zone location. D, Heat maps of the mean entry probability across all false exits (1–19) and the exit zone during the probe trial for IH_Saline and IH_MnTMPyP. Comparison of entry probability into the exit zone during the probe trial reveals that IH_MnTMPyP has a greater probability for entering the exit zone when compared with IH_Saline (p = 0.006); ***p < 0.001, *p < 0.05; N.S., p > 0.05.