A behavioral role for dendritic integration:: HCN1 channels constrain spatial inputs to distal dendrites memory and plasticity at of CA1 pyramidal neurons
A behavioral role for dendritic integration:: HCN1 channels constrain spatial inputs to distal dendrites memory and plasticity at of CA1 pyramidal neurons
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DOI：
10.1016/s0092-8674(04)01055-4
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发表时间：
2004-11-24
期刊：
影响因子：
64.5
通讯作者：
Morozov, A
中科院分区：
文献类型：
--
作者：
Nolan, MF;Malleret, G;Morozov, A
长期突触可塑性作为学习和记忆的细胞基质的重要性是众所周知的。相比之下，人们对整合突触信息的电压门控离子通道如何调节学习和记忆知之甚少。我们使用 HCN1 基因全面或前脑限制性敲除的小鼠研究了这个问题，我们发现 HCN1 基因编码超极化激活内向电流 (I-h) 的主要成分，并且是海马 CA1 锥体细胞树突整合的重要决定因素。从前脑神经元中删除HCN1可以增强海马依赖性学习和记忆，增强θ振荡的力量，并增强CA1锥体神经元远端树突直接穿通路径输入的长时程增强（LTP），但对更近端Schaffer侧支输入的LTP影响不大。我们认为 HCN1 通道通过调节远端突触输入到锥体细胞的树突整合来限制学习和记忆。
The importance of long-term synaptic plasticity as a cellular substrate for learning and memory is well established. By contrast, little is known about how learning and memory are regulated by voltage-gated ion channels that integrate synaptic information. We investigated this question using mice with general or forebrain-restricted knockout of the HCN1 gene, which we find encodes a major component of the hyperpolarization-activated inward current (I-h) and is an important determinant of dendritic integration in hippocampal CA1 pyramidal cells. Deletion of HCN1 from forebrain neurons enhances hippocampal-dependent learning and memory, augments the power of theta oscillations, and enhances long-term potentiation (LTP) at the direct perforant path input to the distal dendrites of CA1 pyramidal neurons, but has little effect on LTP at the more proximal Schaffer collateral inputs. We suggest that HCN1 channels constrain learning and memory by regulating dendritic integration of distal synaptic inputs to pyramidal cells.