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. 2009 Mar 30;1(2):97–115.

Table 3.

Summary of caspase activation after experimental seizure-induced neuronal death and the effects of caspase inhibitors on seizure-damage

Inhibitor Model Time period and method of assessment Hippocampal TUNEL counts Hippocampal CA3 survivala References
Caspase-1 ESA n.d. n.d. No effectb [77]
Caspase-3 IAK 4-24 h (WB, A) n.d. Increased [60]
ESA n.d. n.d. Increased [77]
Caspase-8 IAK 0-72 h (WB, A) Reduced Increased [67]
IAK 0-72 h (WB) Reduced Increased [61]
Caspase-9 IAK 4-72 h (WB, A) Reduced Increased [64]
IAK 4-72 h (WB) Reduced Increased [117]
ESA n.d. n.d. Increased [77]
viral p35 SK 8 h (A) Reduced n.d. [66]

Data are for CA3 subfield of the hippocampus. Inhibitors were: Ac-YVAD-cmk (caspase-1), z-DEVD-fmk (caspase-3), z-IETD-fmk (caspase-8) and z-LEHD-fmk (caspase-9).

a

Assessments made on either degenerating or remaining neurons in the CA3 part of the hippocampus.

b

Tendency to neuroprotection seen in dentate gyrus. Key: n.d., not determined; ESA, electrical stimulation of the amygdala; IAK, intra-amygdala kainic acid; SK, systemic kainic acid; WB, Western blot, A, enzyme assay.