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Fig. 7 | Molecular Medicine

Fig. 7

From: BAX Contributes to Apoptotic-Like Death Following Neonatal Hypoxia-Ischemia: Evidence for Distinct Apoptosis Pathways

Fig. 7

Caspase-8 activation following neonatal H-I is present in both bax +/− and bax −/− mice. P7 mice were subjected to H-I and 24 hours later, sections were labeled with antibodies to activated caspase-3 and activated caspase-8 and assessed by double label immunofluorescence and confocal microscopy. There was little staining of cells in the unlesioned right hippocampus in either bax +/− (A) or bax −/− mice (B). In contrast, in the lesioned (left) hippocampus (CA3 shown here), there were cells which labeled with antibodies to activated caspase-3 (red), activated caspase-8 (green), or were labeled with both antibodies (yellow) (C–F). Most cells that were labeled by antibodies to activated caspase-8 were also stained by antibodies to activated caspase-3 (arrows, C–F). There were also cells, particularly in the bax +/− mice, which only labeled with antibodies to activated caspase-3 (arrowheads, C, E). Scale bar in D equals 50 µm for A–D. Scale bar in F equals 10 µm for E, F. In G, the density of activated caspase-8-IR cells (per 0.023 mm2) in the CA3 region of the lesioned hippocampus was compared in bax +/− (n = 5) vs. bax −/− (n = 5) mice. The same mice analyzed for CA1 neurons in Fig. 3 were utilized in this experiment. There was no significant difference between the groups. The total number of remaining CA3 neurons as well as the % CA3 cell loss (right-left/right X 100) in both groups was also determined in the uninjured (right) and injured (left) hippocampus of these animals. Number of CA3 neurons (mean +/− SEM): bax +/−, right: 98,240 +/− 11,640; bax −/−, right: 100,800 +/− 11,900; bax +/−, left: 42,430 +/− 11,040; bax −/−, left: 42,530 +/− 15,160). % CA3 cell loss (mean +/− SEM): bax +/− 56.1 +/− 12.9; bax −/− 58.4 +/− 9.7.

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