Molinari S, Battini R, Ferrari S, Pozzi L, Killcross A S, Robbins T W, Jouvenceau A, Billard J M, Dutar P, Lamour Y, Baker W A, Cox H, Emson P C
Dipartimento di Scienze Biomediche, Sezione di Chimica Biologica, Universita di Modena, Italy.
Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):8028-33. doi: 10.1073/pnas.93.15.8028.
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 time 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 D28K, which is abundant in many neurons, including the CA1 pyramidal cells of the hippocampus, transgenic mice deficient in calbindin D28K 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.
钙离子流入突触后神经元很可能是记忆形成过程中的一个重要事件。在神经细胞用于改变细胞内钙峰时间进程或大小的机制中，有胞质钙结合或“缓冲”蛋白。为了研究其中一种蛋白——钙结合蛋白D28K（在包括海马体CA1锥体细胞在内的许多神经元中含量丰富）在记忆形成中的作用，人们培育出了缺乏钙结合蛋白D28K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，并且无法维持长时程增强。这些结果表明，钙结合蛋白D28K在神经元钙信号的时间延长方面发挥作用，从而激活记忆功能背后的钙依赖性细胞内信号通路。
