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. 2008 Feb;172(2):454–469. doi: 10.2353/ajpath.2008.070876

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The apoptotic pathway is inhibited in the neonatal hippocampus after H/I injury by the Atg7 deficiency. A–D: Triple staining for cleaved caspase-3 (Casp3) (A, C), TUNEL (A, C), and DAPI (B, D) in the ipsilateral hippocampi of Atg7-deficient (Atg7^flox/flox; Nes) (A, B) and control littermate (Atg7^flox/flox) (C, D) mouse brains 24 hours after H/I injury. E: The neuronal cell architecture as well as morphological features of the neurons appeared intact in the hippocampal pyramidal layer of an Atg7-deficient mouse brain 24 hours after H/I injury. F: Western blotting of caspases-3 and -7 in the ipsilateral (IL) and contralateral hippocampi of littermate control (Atg7^flox/flox) and Atg7-deficient (Atg7^flox/flox; Nes) mouse brains 8 hours after H/I injury. Cleaved caspase-3, but not caspase-7, was detected only in the control IL hippocampus. GAPDH was used as a loading control. G: The DNA fragmentation in the ipsilateral (IL) and contralateral (CL) hippocampi from Atg7-deficient (Atg7^flox/flox; Nes) and littermate (Atg7^flox/flox) mouse brains 24 hours after H/I injury. Scale bars: 20 μm (A–D); 5 μm (E).