12月29日,，據(jù)《每日科學(xué)》報道,，神經(jīng)膠質(zhì)細胞，以希臘字母"glue（膠水）"命名,，它將大腦中的神經(jīng)元聚攏并保護這些決定我們思想和行為的細胞,。但長久以來，科學(xué)家一直對它們在決定大腦學(xué)習(xí)和記憶的活動中的突出作用感到困惑?，F(xiàn)在,，特拉維夫大學(xué)的研究人員說，神經(jīng)膠質(zhì)細胞是大腦的可塑性的核心--大腦是如何適應(yīng),、學(xué)習(xí),、儲存信息。
據(jù)特拉維夫大學(xué)天文物理和電氣工程博士Maurizio De Pitta說,，神經(jīng)膠質(zhì)細胞遠不止是支持大腦細胞這么簡單,。神經(jīng)膠質(zhì)細胞內(nèi)的一個機制同樣在為學(xué)習(xí)的目的進行信息歸類，De Pitta說,，"神經(jīng)膠質(zhì)細胞就像大腦的管理者,，通過調(diào)節(jié)突觸，它們控制著神經(jīng)元之間的信息傳輸,，影響大腦處理信息及學(xué)習(xí),。"
De Pitta的研究，由他的導(dǎo)師-特拉維夫大學(xué)教授Eshel Ben-Jacob領(lǐng)導(dǎo),，同時與索爾克研究所和圣地亞哥加利福尼亞大學(xué)的Vladislay Volman,、法國里昂大學(xué)的Hugues Berry共同協(xié)作,，開發(fā)出了首個電腦模型，整合了神經(jīng)膠質(zhì)細胞對突觸信息傳遞的影響,。在PLoS計算生物學(xué)期刊中詳細介紹,，這個模型也可以應(yīng)用于基于大腦網(wǎng)絡(luò)結(jié)構(gòu)的技術(shù)領(lǐng)域如芯片和電腦軟件，Ben-Jacob教授說,，輔助阿爾茨海默氏癥和癲癇等大腦失調(diào)癥的研究,。
調(diào)節(jié)大腦的"社會網(wǎng)絡(luò)"
大腦是由2類主要的細胞組成：神經(jīng)元和神經(jīng)膠質(zhì)細胞。神經(jīng)元熄滅諸如決定我們思想和行為的信息,，通過突觸將這些信息從一個神經(jīng)元傳遞到另一個神經(jīng)元,，De Pitta解釋說?？茖W(xué)家推論,，記憶和學(xué)習(xí)是由突觸的活動決定，因為它們是"可塑的",，具有適應(yīng)不同刺激的能力,。但Ben-Jacob和他的同事們推測，神經(jīng)膠質(zhì)細胞對于大腦如何工作更加重要,。神經(jīng)膠質(zhì)細胞大量存在于大腦的海馬和皮層,，它們是大腦的2個部分，最大程度地控制著大腦處理信息,、學(xué)習(xí)和記憶的能力,。事實上，每一個神經(jīng)元,，都有2-5個神經(jīng)膠質(zhì)細胞,。合并之前的實驗數(shù)據(jù)，研究人員有能力建立起一個模型來解決這個難題,。
大腦就像個社會網(wǎng)絡(luò),，Ben-Jacob教授說。信息可能起源于神經(jīng)元,，它使用突觸作為它們的傳輸工具,，但神經(jīng)膠質(zhì)細胞發(fā)揮著總仲裁者的作用，調(diào)控發(fā)送哪些信息及何時發(fā)送,。這些細胞要么促進信息的傳遞,，或要么減緩如果突觸過于活躍的話。這使得神經(jīng)膠質(zhì)細胞充當(dāng)了我們學(xué)習(xí)和記憶過程的監(jiān)護人,，他指出,，策劃著信息的傳輸達到最佳的大腦功能。
新的大腦激發(fā)技術(shù)和療法
該小組的研究結(jié)果對于許多腦部疾病來說具有非常重要的意義,。幾乎所有的神經(jīng)退行性疾病都與膠質(zhì)細胞有關(guān),，Ben-Jacob教室指出,。例如，在癲癇中,，一處神經(jīng)元的活動過于活躍并壓制了其他地方的正?；顒印．?dāng)神經(jīng)膠質(zhì)細胞不能準(zhǔn)確的調(diào)節(jié)突觸傳遞時,，這種情況就發(fā)生了,。此外，當(dāng)大腦活動減緩時,，神經(jīng)膠質(zhì)細胞促進信息的傳輸,，保持各個神經(jīng)元之間連接的"活度"。
該模型為了解大腦如何行使功能提供了一個"新觀點",。盡管該項研究還在繼續(xù),，2項實驗工作似乎支持了這個模型的預(yù)測。"越來越多的科學(xué)家開始認識到這樣一個事實,，那就是,，你需要神經(jīng)膠質(zhì)細胞去執(zhí)行那些單靠神經(jīng)元細胞不能以有效的方式完成的任務(wù)，"De Pitta說,。該模型將提供一個新的工具,，來修正計算神經(jīng)科學(xué)理論，并引發(fā)更切實際的腦啟發(fā)算法和芯片,，來模擬神經(jīng)網(wǎng)絡(luò),。（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.
