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. Author manuscript; available in PMC: 2012 Jul 3.
Published in final edited form as: Brain Res. 2009 May 3;1279:139–146. doi: 10.1016/j.brainres.2009.04.045

Fig. 2. Histologic neuronal and axonal damages in the hippocampal CA1 region following global cerebral ischemia caused by cardiac arrest and resuscitation (CAR).

Fig. 2

Representative sections of cresyl violet staining (A1–5) and immunostained sections of MAP2 (B1–5 and C1–5), βAPP (D1–5), and Iba-1 (E1–5) in the CA1 in the Sham, Isc1, Isc2, Edv0, and Edv60 groups are depicted. A1: Normal pyramidal neurons in the Sham group. A2 and A3: Typical appearance of neuronal damage 1 week (Isc1) and 2 weeks (Isc2) after CAR, respectively. A4 and A5: Reduction of neuronal damage by edaravone administered immediately (Edv0) and 60 min (Edv60) after CAR, respectively. B1: Normal MAP2 expression in the Sham group. A white square shows the region of predetermined area for the neuronal perikaryal and axonal damages evaluation. B2 and B3: Extensive decrease in MAP2 expression after CAR in the Isc1 and Isc2 groups, respectively. B4 and B5: Mitigation of decrease in MAP2 expression by edaravone in the Edv0 and Edv60 groups. C: MAP2 expression as in B at a higher magnification. D1 and D2: Normal detection level of the βAPP accumulation in the Sham and Isc1 groups, respectively, one week after CAR. D3: Extensive granular βAPP deposition 2 weeks after CAR in the Isc2 group. D4 and D5: Mitigation of βAPP accumulation in the edaravone-treated groups. E1: Scattered ramified microglias are found in the Sham group. E2 and E3: Dense accumulation of ameboid microglias 1 week and 2 weeks after CAR. E4: Microglial activation is slightly suppressed by edaravone administered immediately after CAR. E5: Microglial activation is markedly suppressed by edaravone administered 60 minutes after CAR. Scale Bar: 50 μm (A, C, D, and E); 1 mm (B).