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. 2016 Feb 3;10:14. doi: 10.3389/fncel.2016.00014

Figure 2.

Figure 2

Organotypic hippocampal slice cultures (OHSCs) isolated from BID deficient mice show protection in response to oxygen-glucose deprivation (OGD). The slices were sham-exposed or subjected to OGD conditions for 180 min in the absence or the presence of 10 μM MK-801 and allowed to recover for 24 h. (A) Representative images of OHSCs derived from BID-KO and WT mice. (B) Quantification of injury assessed by PI staining 24 h post-treatment in the CA1 subfield of the hippocampal slices. In the absence of MK-801, BID deficiency protected against neuronal injury (*p = 0.024). Note the protection exerted by MK-801 against OGD-induced neuronal injury of WT OHSCs. In BID-KO slice cultures MK-801 failed to reduce OGD-induced neuronal injury. Scale bar: 100 μm, (n = 3–7 in each group, 2-way ANOVA, mean ± SD).