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首页> 外文期刊>Molecular and Cellular Biology >Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase α-Deficient Mice
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Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase α-Deficient Mice

机译：Ca2 + /钙调蛋白激酶激酶α缺陷型小鼠巴甫洛夫恐惧条件的长期记忆缺陷。

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Signaling by the Ca2+/calmodulin kinase (CaMK) cascade has been implicated in neuronal gene transcription, synaptic plasticity, and long-term memory consolidation. The CaM kinase kinase α (CaMKKα) isoform is an upstream component of the CaMK cascade whose function in different behavioral and learning and memory paradigms was analyzed by targeted gene disruption in mice. CaMKKα mutants exhibited normal long-term spatial memory formation and cued fear conditioning but showed deficits in context fear during both conditioning and long-term follow-up testing. They also exhibited impaired activation of the downstream kinase CaMKIV/Gr and its substrate, the transcription factor cyclic AMP-responsive element binding protein (CREB) upon fear conditioning. Unlike CaMKIV/Gr-deficient mice, the CaMKKα mutants exhibited normal long-term potentiation and normal levels of anxiety-like behavior. These results demonstrate a selective role for CaMKKα in contextual fear memory and suggest that different combinations of upstream and downstream components of the CaMK cascade may serve distinct physiological functions.
机译：Ca 2 + /钙调蛋白激酶（CaMK）级联的信号传导与神经元基因转录，突触可塑性和长期记忆巩固有关。 CaM激酶激酶α（CaMKKα）亚型是CaMK级联反应的上游成分，通过小鼠中的靶向基因破坏来分析其在不同行为，学习和记忆范例中的功能。 CaMKKα突变体表现出正常的长期空间记忆形成和暗示恐惧条件，但在条件条件和长期随访测试中表现出背景恐惧的缺陷。他们还表现出对下游激酶CaMKIV / Gr及其底物，即恐惧调节后的转录因子环AMP响应元件结合蛋白（CREB）的激活受损。与CaMKIV / Gr缺陷小鼠不同，CaMKKα突变体表现出正常的长期增强作用和正常水平的焦虑样行为。这些结果证明了CaMKKα在背景恐惧记忆中的选择性作用，并表明CaMK级联的上游和下游成分的不同组合可能发挥不同的生理功能。

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