Cytephysiological investigation for abnormal Ca^<2+> metabolism in delayed neuronal death

IP_33激酶基因敲除小鼠的功能变化为了研究IP_4在正常或病理状态下的作用，我们使用IP_33激酶基因敲除小鼠进行实验。双侧颈总动脉阻断10 min后，基因敲除小鼠和枯萎型小鼠的病理学变化无显著性差异。海马脑片缺氧缺糖诱导的Rhod 2成像中钙增加也无差异。在被动回避实验中，IP_33激酶基因敲除的小鼠表现出明显较差的结果。缝隙连接在脑缺血中的作用本研究旨在探讨差距连接蛋白Cx 32（由少突胶质细胞和/或中间神经元表达）、Cx 36（由中间神经元和某些锥体神经元表达）和Cx 43（由星形胶质细胞表达）在确定神经元死亡的细胞特异性模式中的作用。 ...更多信息 全脑缺血后小鼠海马中h的变化。通过北方印迹分析和原位杂交评估，全脑缺血并没有显著改变易损CA 1中Cx 32、Cx 36和Cx43 mRNA的表达。全脑缺血诱导Cx 32和Cx 36，但不是Cx43，蛋白丰度在CA 1神经元死亡的发病前，通过Western印迹分析评估的选择性增加。Cx 32和Cx 36表达的增加是在palvalbumine阳性抑制海马CA 1区的中间神经元，通过双重免疫荧光法进行评估。CA 3区和齿状回的三种连接蛋白的表达在所有检测时间均无变化。连接蛋白在相应mRNA不发生变化的情况下发生变化的发现与Cx 32和Cx 36在翻译和/或翻译后水平表达的调节一致。Cx 32（Y/）空小鼠表现出增强的脆弱性，短暂的缺血性损伤，Cx 32间隙连接在神经元存活的作用一致。这些研究结果表明，Cx 32和Cx 36间隙连接有助于GABA能中间神经元的存活和抵抗的机制，从而定义了全脑缺血诱导的神经元死亡的细胞特异性模式。少

Functional changes in IP_33kinase knock-out miceTo investigate the role of IP4 in the normal or the pathological conditions, we performed experiments using IP_33kinase knock-out mice. The vulnerability to global ischemia by 10 min bilateral common carotid occlusion, no differences was detected in pathological study between knock-out mice and the wilt type. Calcium increase in Rhod2 imaging induced by oxygen-glucose deprivation on hippocampal slice also showed no differences. In passive avoidance test IP_33kinase knock-out mice showed significantly poorer results. These results suggest that IP4 plays some role in keeping memory.The role of gap junction in cerebral ischemiaThe present study was undertaken to examine the hypothesis that the gap junctional proteins Cx (connexin) 32 (expressed by oligodendrocytes and/or interneurons), Cx36 (expressed by interneurons and some pyramidal neurons) and Cx43 (expressed by astrocytes) play a role in defining cell-specific patterns of neuronal deat … More h in the hippocampus after global ischemia in mice. Global ischemia did not significantly alter Cx32, Cx36 and Cx43 mRNA expression in the vulnerable CA1, as assessed by Northern blot analysis and in situ hybridization. Global ischemia induced a selective increase in Cx32 and Cx36, but not Cx43, protein abundance in CA1 prior to the onset of neuronal death, as assessed by Western blot analysis. The increase in Cx32 and Cx36 expression was in palvalbumine positive inhibitory interneurons of the hippocampal CA1, as assessed by double immunofluorescence. Abundance of the three connexin proteins was unchanged in CA3 and dentate gyrus at all times examined. The finding that connexin proteins change in the absence of a change in the corresponding mRNAs is consistent with the regulation of Cx32 and Cx36 expression at the translational and/or post-translational levels. Cx32 (Y/) null mice exhibited enhanced vulnerability to brief ischemic insults, consistent with a role for Cx32 gap junctions in neuronal survival. These findings suggest a mechanism by which Cx32 and Cx36 gap junctions contribute to the survival and resistance of GABAergic interneurons, thereby defining cell-specific patterns of global ischemia-induced neuronal death. Less