Cholesterol depletion inhibits electrophysiological changes induced by anoxia in CA1 region of rat hippocampal slices

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• 作者：Stefano Rufini ; Daniele Grossi ; Paolo Luly ; Virginia Tancredi ; Claudio Frank ; Giovanna D'Arcangelo
• 关键词：Ischemia ; Synaptic transmission ; LTP ; Hippocampal slice ; Anoxia ; Aglycemia ; Methyl-beta-cyclodextrin ; Cholesterol ; Lipid raft ; Kainate receptor
• 刊名：Brain Research
• 出版年：2009
• 出版时间：28 October 2009
• 年：2009
• 卷：1298
• 期：Complete
• 页码：178-185
• 全文大小：490 K

文摘

The hyper-activation of glutamate receptors is a key event in the degenerative processes triggered by ischemia in the brain. Several types of these receptors reside in cholesterol–sphingomyelin rich domains of post-synaptic plasma membranes and have been described to be sensitive to cholesterol depletion. Hence we investigated, by extracellular recordings, the effect of cholesterol depletion on population spikes (PS) during ischemia-like conditions in the CA1 region of rat hippocampal slices using the cholesterol-depleting agent methyl-beta-cyclodextrin (MβCD). Results obtained demonstrate that MβCD prevents the changes induced by anoxic insult, i.e., depression of the population spike amplitude and insurgence of ischemic long-term potentiation. Furthermore cholesterol depletion prevents the disappearance of population spike induced by anoxia/aglycemia during kainate perfusion. Our data suggest a possible role of MβCD in preventing the pathological changes in synaptic activity induced by ischemia and indicate that manipulation of lipid components of membrane rafts might provide a new approach for the treatment of ischemia.