Control of synaptic strength by glial TNFalpha.
Control of synaptic strength by glial TNFalpha.
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DOI：
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发表时间：
2002
期刊：
影响因子：
56.9
通讯作者：
E. Beattie;D. Stellwagen;W. Morishita;J. Bresnahan;Byeong Keun Ha;M. von Zastrow;M. Beattie;R. Malenka-R
中科院分区：
文献类型：
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作者：
E. Beattie;D. Stellwagen;W. Morishita;J. Bresnahan;Byeong Keun Ha;M. von Zastrow;M. Beattie;R. Malenka-R
大脑中突触功效的活动依赖性调制有助于神经回路发育和经验依赖性可塑性。虽然神经胶质细胞受到活动的影响，并包裹突触，但它们对突触强度的影响在很大程度上被忽视了。在这里，我们表明，神经胶质细胞产生的蛋白质，肿瘤坏死因子α（TNF α），通过增加AMPA受体的表面表达增强突触的功效。阻止内源性TNF α的作用具有相反的效果。因此，TNF α的持续存在是保持兴奋性突触的突触强度所必需的。通过其对AMPA受体运输的影响，TNF α可能在突触可塑性和调节对神经损伤的反应中发挥作用。
Activity-dependent modulation of synaptic efficacy in the brain contributes to neural circuit development and experience-dependent plasticity. Although glia are affected by activity and ensheathe synapses, their influence on synaptic strength has largely been ignored. Here, we show that a protein produced by glia, tumor necrosis factor alpha (TNFalpha), enhances synaptic efficacy by increasing surface expression of AMPA receptors. Preventing the actions of endogenous TNFalpha has the opposite effects. Thus, the continual presence of TNFalpha is required for preservation of synaptic strength at excitatory synapses. Through its effects on AMPA receptor trafficking, TNFalpha may play roles in synaptic plasticity and modulating responses to neural injury.