Neuronal Plasticity Promoted by Glia

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Abstract

Tumor necrosis factor-α (TNF-α), otherwise known as a proinflammatory cytokine, turns out to be active on a continual basis in the nervous system. Beattie et al., studied synaptic function in cultured hippocampal neurons and hippocampal brain slices and showed that TNF-α promotes expression of a neurotransmitter receptor on the cell surfaces at synapses. TNF-α is required continuously, suggesting that it may contribute to rapid adjustment of receptor levels at a synapse. TNF-α is supplied by affiliated glial cells, once again reminding us that the glial cells, previously thought to be rather passive support partners, are important behind-the-scenes participants in neuronal function. E. C. Beattie, D. Stellwagen, W. Morishita, J. C. Bresnahan, B. K. Ha, M.Von Zastrow, M. S. Beattie, R. C. Malenka, Control of synaptic strength by glial TNF-α. Science 295, 2282-2285 (2002). [Abstract] [Full Text]
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胶质细胞促进神经元可塑性
肿瘤坏死因子-α (TNF-α),也被称为促炎细胞因子,在神经系统中持续活跃。Beattie等研究了培养海马神经元和海马脑切片的突触功能,发现TNF-α促进突触细胞表面一种神经递质受体的表达。TNF-α是持续需要的,这表明它可能有助于突触中受体水平的快速调节。TNF-α是由附属的神经胶质细胞提供的,这再次提醒我们,神经胶质细胞,以前被认为是相当被动的支持伙伴,在幕后是重要的神经元功能参与者。E. C. Beattie, D. Stellwagen, W. Morishita, J. C. Bresnahan, B. K. Ha, M. von Zastrow, M. S. Beattie, R. C. Malenka,神经胶质细胞TNF-α对突触强度的控制。科学295,2282-2285(2002)。【摘要】【全文】
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