12月29日，据《每日科学》报道，神经胶质细胞，以希腊字母"glue（胶水）"命名，它将大脑中的神经元聚拢并保护这些决定我们思想和行为的细胞。但长久以来，科学家一直对它们在决定大脑学习和记忆的活动中的突出作用感到困惑。现在，特拉维夫大学的研究人员说，神经胶质细胞是大脑的可塑性的核心--大脑是如何适应、学习、储存信息。
据特拉维夫大学天文物理和电气工程博士Maurizio De Pitta说，神经胶质细胞远不止是支持大脑细胞这么简单。神经胶质细胞内的一个机制同样在为学习的目的进行信息归类，De Pitta说，"神经胶质细胞就像大脑的管理者，通过调节突触，它们控制着神经元之间的信息传输，影响大脑处理信息及学习。"
De Pitta的研究，由他的导师-特拉维夫大学教授Eshel Ben-Jacob领导，同时与索尔克研究所和圣地亚哥加利福尼亚大学的Vladislay Volman、法国里昂大学的Hugues Berry共同协作，开发出了首个电脑模型，整合了神经胶质细胞对突触信息传递的影响。在PLoS计算生物学期刊中详细介绍，这个模型也可以应用于基于大脑网络结构的技术领域如芯片和电脑软件，Ben-Jacob教授说，辅助阿尔茨海默氏症和癫痫等大脑失调症的研究。
调节大脑的"社会网络"
大脑是由2类主要的细胞组成：神经元和神经胶质细胞。神经元熄灭诸如决定我们思想和行为的信息，通过突触将这些信息从一个神经元传递到另一个神经元，De Pitta解释说。科学家推论，记忆和学习是由突触的活动决定，因为它们是"可塑的"，具有适应不同刺激的能力。但Ben-Jacob和他的同事们推测，神经胶质细胞对于大脑如何工作更加重要。神经胶质细胞大量存在于大脑的海马和皮层，它们是大脑的2个部分，最大程度地控制着大脑处理信息、学习和记忆的能力。事实上，每一个神经元，都有2-5个神经胶质细胞。合并之前的实验数据，研究人员有能力建立起一个模型来解决这个难题。
大脑就像个社会网络，Ben-Jacob教授说。信息可能起源于神经元，它使用突触作为它们的传输工具，但神经胶质细胞发挥着总仲裁者的作用，调控发送哪些信息及何时发送。这些细胞要么促进信息的传递，或要么减缓如果突触过于活跃的话。这使得神经胶质细胞充当了我们学习和记忆过程的监护人，他指出，策划着信息的传输达到最佳的大脑功能。
新的大脑激发技术和疗法
该小组的研究结果对于许多脑部疾病来说具有非常重要的意义。几乎所有的神经退行性疾病都与胶质细胞有关，Ben-Jacob教室指出。例如，在癫痫中，一处神经元的活动过于活跃并压制了其他地方的正常活动。当神经胶质细胞不能准确的调节突触传递时，这种情况就发生了。此外，当大脑活动减缓时，神经胶质细胞促进信息的传输，保持各个神经元之间连接的"活度"。
该模型为了解大脑如何行使功能提供了一个"新观点"。尽管该项研究还在继续，2项实验工作似乎支持了这个模型的预测。"越来越多的科学家开始认识到这样一个事实，那就是，你需要神经胶质细胞去执行那些单靠神经元细胞不能以有效的方式完成的任务，"De Pitta说。该模型将提供一个新的工具，来修正计算神经科学理论，并引发更切实际的脑启发算法和芯片，来模拟神经网络。（生物谷bioon.com）
doi:10.1371/journal.pcbi.1002293
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A Tale of Two Stories: Astrocyte Regulation of Synaptic Depression and Facilitation
Maurizio De Pittà, Vladislav Volman, Hugues Berry,Eshel Ben-Jacob
Abstract ：Short-term presynaptic plasticity designates variations of the amplitude of synaptic information transfer whereby the amount of neurotransmitter released upon presynaptic stimulation changes over seconds as a function of the neuronal firing activity. While a consensus has emerged that the resulting decrease (depression) and/or increase (facilitation) of the synapse strength are crucial to neuronal computations, their modes of expression in vivo remain unclear. Recent experimental studies have reported that glial cells, particularly astrocytes in the hippocampus, are able to modulate short-term plasticity but the mechanism of such a modulation is poorly understood. Here, we investigate the characteristics of short-term plasticity modulation by astrocytes using a biophysically realistic computational model. Mean-field analysis of the model, supported by intensive numerical simulations, unravels that astrocytes may mediate counterintuitive effects. Depending on the expressed presynaptic signaling pathways, astrocytes may globally inhibit or potentiate the synapse: the amount of released neurotransmitter in the presence of the astrocyte is transiently smaller or larger than in its absence. But this global effect usually coexists with the opposite local effect on paired pulses: with release-decreasing astrocytes most paired pulses become facilitated, namely the amount of neurotransmitter released upon spike i+1 is larger than that at spike i, while paired-pulse depression becomes prominent under release-increasing astrocytes. Moreover, we show that the frequency of astrocytic intracellular Ca2+ oscillations controls the effects of the astrocyte on short-term synaptic plasticity. Our model explains several experimental observations yet unsolved, and uncovers astrocytic gliotransmission as a possible transient switch between short-term paired-pulse depression and facilitation. This possibility has deep implications on the processing of neuronal spikes and resulting information transfer at synapses.
Author Summary ：Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neuronal activity. Because it admittedly underlies learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. Short-term presynaptic plasticity refers to changes occurring over short time scales (milliseconds to seconds) that are mediated by frequency-dependent modifications of the amount of neurotransmitter released by presynaptic stimulation. Recent experiments have reported that glial cells, especially hippocampal astrocytes, can modulate short-term plasticity, but the mechanism of such modulation is poorly understood. Here, we explore a plausible form of modulation of short-term plasticity by astrocytes using a biophysically realistic computational model. Our analysis indicates that astrocytes could simultaneously affect synaptic release in two ways. First, they either decrease or increase the overall synaptic release of neurotransmitter. Second, for stimuli that are delivered as pairs within short intervals, they systematically increase or decrease the synaptic response to the second one. Hence, our model suggests that astrocytes could transiently trigger switches between paired-pulse depression and facilitation. This property explains several challenging experimental observations and has a deep impact on our understanding of synaptic information transfer.
