Trace eyeblink conditioning requires the hippocampus but not autophosphorylation of alphaCaMKII in mice.
Trace eyeblink conditioning requires the hippocampus but not autophosphorylation of alphaCaMKII in mice.
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DOI：
10.1101/lm.90205
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发表时间：
2005-05
影响因子：
2
通讯作者：
M. Ohno;Wilbur Tseng;Alcino J. Silva;J. Disterhoft
中科院分区：
文献类型：
--
作者：
M. Ohno;Wilbur Tseng;Alcino J. Silva;J. Disterhoft
关于时间联想学习背后的信号机制，人们知之甚少。在这里，我们显示了具有阻止AlphaCaMKII(AlphaCaMKII(T286A))自动磷酸化的靶点突变的小鼠正常学习痕迹眨眼条件反射。这与在alphaCaMKII(T286A)突变体中观察到的水迷宫中严重受损的空间学习和上下文恐惧条件反射形成了鲜明的对比。重要的是，海马区损伤损害了阿尔法CaMKII(T286A)小鼠的痕量眨眼条件反射，这表明海马区αCaMKII非依赖机制可能起作用。这些结果表明，时间联想学习背后的海马区信号机制可能不同于空间和语境学习。
Little is known about signaling mechanisms underlying temporal associative learning. Here, we show that mice with a targeted point mutation that prevents autophosphorylation of alphaCaMKII (alphaCaMKII(T286A)) learn trace eyeblink conditioning normally. This forms a sharp contrast to the severely impaired spatial learning in the water maze and contextual fear conditioning observed in alphaCaMKII(T286A) mutants. Importantly, hippocampal lesions impaired trace eyeblink conditioning in alphaCaMKII(T286A) mice, suggesting a potential role of hippocampal alphaCaMKII-independent mechanisms. These results indicate that hippocampal signaling mechanisms that underlie temporal associative learning as assessed by trace eyeblink conditioning may differ from those of spatial and contextual learning.