Deficits in memory and hippocampal long-term potentiation in mice with reduced calbindin D-28K expression
Deficits in memory and hippocampal long-term potentiation in mice with reduced calbindin D-28K expression
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DOI：
10.1073/pnas.93.15.8028
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发表时间：
1996-07-23
影响因子：
11.1
通讯作者：
Emson, PC
中科院分区：
文献类型：
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作者：
Molinari, S;Battini, R;Emson, PC
钙流入突触后神经元可能是记忆形成过程中的一个重要事件。神经细胞可能通过胞质钙结合或“缓冲”蛋白来改变细胞内钙峰的过程或大小。calbindin D-28K存在于许多神经元中，包括海马的CA1锥体，为了研究其中一种蛋白质calbindin D-28K在记忆形成中的作用，研究人员创造了缺乏calbindin D-28K的转基因小鼠。这些小鼠在空间学习范式中表现出选择性损伤，无法维持长期增强。这些结果表明calbindin D28K蛋白在暂时延长神经元钙信号中的作用，允许激活记忆功能基础上的钙依赖性细胞内信号通路。
The influx of calcium into the postsynaptic neuron is likely to be an important event in memory formation. Among the mechanisms that nerve cells may use to alter the Lime course or size of a spike of intracellular calcium are cytosolic calcium binding or ''buffering'' proteins. To consider the role in memory formation of one of these proteins, calbindin D-28K, which is abundant in many neurons, including the CA1 pyramidal tells of the hippocampus, transgenic mice deficient in calbindin D-28K have been created. These mice show selective impairments in spatial learning paradigms and fail to maintain long-term potentiation. These results suggest a role for calbindin D28K protein in temporally extending a neuronal calcium signal, allowing the activation of calcium-dependent intracellular signaling pathways underlying memory function.