Subregion-specific vulnerability to endoplasmic reticulum stress-induced neurotoxicity in rat hippocampal neurons.
作者： Yasuhiro Kosuge , Toru Imai , Mitsuru Kawaguchi , Tetsuroh Kihara , Kumiko Ishige
DOI: 10.1016/J.NEUINT.2007.12.010
关键词: Hippocampal formation 、 Neuroscience 、 Propidium iodide 、 Neuron 、 Neurotoxicity 、 Biology 、 Neurodegeneration 、 Endoplasmic reticulum 、 Cell biology 、 Hippocampus 、 Dentate gyrus
摘要: It is well known that in certain disease states, including ischemia and Alzheimer's disease, neurodegeneration occurs the hippocampus vulnerability to neuronal death area dependent. The present study investigated mechanism of area-dependent under endoplasmic reticulum stress conditions induced by tunicamycin (TM), using rat organotypic hippocampal cultures (OHC) slices. Analysis propidium iodide uptake showed TM-induced a concentration-dependent manner (20-80 microg/mL) rank order among subregions was dentate gyrus (DG)>CA1>CA3. Results immunohistochemistry slices also procaspase-12-positive cells CA3 were significantly fewer than those CA1 DG. Moreover, procurement neurons areas CA1, DG laser microdissection, followed Western blot analysis, revealed level procaspase-12 lower Pretreatment with z-ATAD-fmk, cell-permeable caspase-12-selective inhibitor attenuated increase PI fluorescence subregion but not CA3. These results suggest TM elicits subregion-specific toxicity OHC at least partly dependent on expression endogenous each hippocampus.
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