Article ID Journal Published Year Pages File Type
6256009 Behavioural Brain Research 2016 8 Pages PDF
Abstract

•We found early immature neuronal death, which was determined by DCX and NeuN-double-staining.•Injection of caspase-3 inhibitor rescued cells from immature neuronal death.•z-DEVD-fmk treatment partially rescued ischemia-induced spatial memory impairment.•Ischemia-induced LTP impairment in the perforant pathway was restored by z-DEVD-fmk treatment.

Memory impairment is a common after an ischemic stroke. While delayed neuronal death in the CA1 region is usually linked to cerebral ischemia-induced memory impairment, the role of early immature neuronal death within the DG region in the memory state of an ischemic stroke model has rarely been studied. Here, we show a partial role of immature neuronal death in memory impairment in a global ischemia model. We found early immature neuronal death, which was determined by DCX and NeuN-double-staining. Injection of z-DEVD-fmk, a caspase-3 inhibitor, into the DG region rescued cells from immature neuronal death in the DG region without affecting delayed neuronal death in the CA1 region of an ischemic brain. Moreover, z-DEVD-fmk treatment partially rescued ischemia-induced spatial memory impairment. We also found that ischemia-induced LTP impairment in the perforant pathway was restored by z-DEVD-fmk treatment. These results suggest that early immature neuronal death is partially involved in ischemia-induced spatial memory impairment.

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Life Sciences Neuroscience Behavioral Neuroscience
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