The h Current Is a Candidate Mechanism for Regulating the Sliding Modification Threshold in a BCM-Like Synaptic Learning Rule
The h Current Is a Candidate Mechanism for Regulating the Sliding Modification Threshold in a BCM-Like Synaptic Learning Rule
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DOI：
10.1152/jn.01129.2009
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发表时间：
2010-08-01
影响因子：
2.5
通讯作者：
Johnston, Daniel
中科院分区：
文献类型：
--
作者：
Narayanan, Rishikesh;Johnston, Daniel
在BCM样突触学习规则中，h电流是调节滑动修改阈值的一种候选机制。神经生理学杂志104：1020-1033,2010。2010年6月16日首次出版；DOI：10.1152/jn.01129.2009。Hebbian突触的可塑性作为一种正反馈机制，可以破坏神经元网络的稳定，除非伴随的平衡这种不稳定的动态平衡过程被激活。在Bienenstock-Cooper-Munro(BCM)类塑性框架中，这种补偿是通过以依赖于活动的方式滑动的修改阈值来实现的。尽管BCM样可塑性框架是理解突触可塑性和化可塑性的有用公式，但这一修饰阈值的活性依赖调节机制仍是一个悬而未决的问题。在这项基于CA1锥体细胞的模拟研究中，我们使用了对其他人提出的钙依赖假说的修改，并表明超极化激活的非特异性阳离子h电流的变化能够改变修改阈值。根据这种变化与h电流变化有关的方向，并得到以前的实验结果的支持，我们认为h电流符合这个修饰阈值的活性依赖调节器的要求。此外，使用相同的框架，我们证明了存在于神经元隔间的多个电压和配体门控离子通道可以通过它们之间的复杂相互作用来调节修饰阈值。我们的结果强调了在生理和病理脑状态下，突触和内在特性/可塑性在调节单个神经元及其网络的学习和动态平衡方面的高度相互依赖。
Narayanan R, Johnston D. The h current is a candidate mechanism for regulating the sliding modification threshold in a BCM-like synaptic learning rule. J Neurophysiol 104: 1020-1033, 2010. First published June 16, 2010; doi: 10.1152/jn.01129.2009. Hebbian synaptic plasticity acts as a positive feedback mechanism and can destabilize a neuronal network unless concomitant homeostatic processes that counterbalance this instability are activated. Within a Bienenstock-Cooper-Munro (BCM)-like plasticity framework, such compensation is achieved through a modification threshold that slides in an activity-dependent fashion. Although the BCM-like plasticity framework has been a useful formulation to understand synaptic plasticity and metaplasticity, a mechanism for the activity-dependent regulation of this modification threshold has remained an open question. In this simulation study based on CA1 pyramidal cells, we use a modification of the calcium-dependent hypothesis proposed elsewhere and show that a change in the hyperpolarization-activated, nonspecific-cation h current is capable of shifting the modification threshold. Based on the direction of such a shift in relation to changes in the h current, and supported by previous experimental results, we argue that the h current fits the requirements for an activity-dependent regulator of this modification threshold. Additionally, using the same framework, we show that multiple voltage-and ligand-gated ion channels present in a neuronal compartment can regulate the modification threshold through complex interactions among themselves. Our results underscore the heavy mutual interdependence of synaptic and intrinsic properties/plasticity in regulating learning and homeostasis in single neurons and their networks under both physiological and pathological brain states.