Modulation of Spike-Timing Dependent Plasticity: Towards the Inclusion of a Third Factor in Computational Models.
Modulation of Spike-Timing Dependent Plasticity: Towards the Inclusion of a Third Factor in Computational Models.
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DOI：
10.3389/fncom.2018.00049
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发表时间：
2018
影响因子：
3.2
通讯作者：
Venance L
中科院分区：
文献类型：
--
作者：
Foncelle A;Mendes A;Jędrzejewska-Szmek J;Valtcheva S;Berry H;Blackwell KT;Venance L
在尖峰时间依赖性可塑性 (STDP) 中，突触强度的变化取决于突触前与突触后尖峰活动的时间。由于 STDP 符合 Hebb 假设，因此它被认为是记忆存储和调用的主要机制之一。 STDP 包含两个符合检测器的系统，其中 N-甲基-D-天冬氨酸受体 (NMDAR) 激活通常被认为是主要组件之一。大量研究揭示了该巧合检测系统的第三个组成部分，即神经调节和塑造 STDP 的神经胶质细胞活动。尽管 STDP 的多巴胺能控制最常被报道，但乙酰胆碱、去甲肾上腺素、一氧化氮 (NO)、脑源性神经营养因子 (BDNF) 或 γ-氨基丁酸 (GABA) 也已被证明可以有效调节 STDP。此外，已经证明星形胶质细胞通过释放或摄取谷氨酸来控制 STDP 表达。在最基本的层面上，STDP 的时间特性预计取决于潜在信号通路的时空动态。然而在大多数情况下，由于技术限制，实验只能间接访问这些途径。通过实验仔细约束的计算模型可以更好地定性了解 STDP 的分子基础及其神经调节剂的调节。最近，钙动力学和信号通路分子的计算模型已开始探索 STDP 在体外和体内类似条件下的出现。这些模型预计将至少部分地更好地再现 STDP 的复杂调节，作为潜在分子途径的新兴特性。阐明 STDP 调制的潜在机制及其对网络动态的影响至关重要，这将有助于更好地理解健康和疾病中记忆存储和回忆的主要机制。
In spike-timing dependent plasticity (STDP) change in synaptic strength depends on the timing of pre- vs. postsynaptic spiking activity. Since STDP is in compliance with Hebb’s postulate, it is considered one of the major mechanisms of memory storage and recall. STDP comprises a system of two coincidence detectors with N-methyl-D-aspartate receptor (NMDAR) activation often posited as one of the main components. Numerous studies have unveiled a third component of this coincidence detection system, namely neuromodulation and glia activity shaping STDP. Even though dopaminergic control of STDP has most often been reported, acetylcholine, noradrenaline, nitric oxide (NO), brain-derived neurotrophic factor (BDNF) or gamma-aminobutyric acid (GABA) also has been shown to effectively modulate STDP. Furthermore, it has been demonstrated that astrocytes, via the release or uptake of glutamate, gate STDP expression. At the most fundamental level, the timing properties of STDP are expected to depend on the spatiotemporal dynamics of the underlying signaling pathways. However in most cases, due to technical limitations experiments grant only indirect access to these pathways. Computational models carefully constrained by experiments, allow for a better qualitative understanding of the molecular basis of STDP and its regulation by neuromodulators. Recently, computational models of calcium dynamics and signaling pathway molecules have started to explore STDP emergence in ex and in vivo-like conditions. These models are expected to reproduce better at least part of the complex modulation of STDP as an emergent property of the underlying molecular pathways. Elucidation of the mechanisms underlying STDP modulation and its consequences on network dynamics is of critical importance and will allow better understanding of the major mechanisms of memory storage and recall both in health and disease.
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影响因子：
4.6
作者：
Cui Y;Prokin I;Mendes A;Berry H;Venance L
通讯作者：
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影响因子：
25
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