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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Selective Activation of Microglia Facilitates Synaptic Strength
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Selective Activation of Microglia Facilitates Synaptic Strength

机译：小胶质细胞的选择性激活促进突触强度。

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摘要

Synaptic plasticity is thought to be initiated by neurons only, with the prevailing view assigning glial cells mere specify supportive functions for synaptic transmission and plasticity. We now demonstrate that glial cells can control synaptic strength independent of neuronal activity. Here we show that selective activation of microglia in the rat is sufficient to rapidly facilitate synaptic strength between primary afferent C-fibers and lamina I neurons, the first synaptic relay in the nociceptive pathway. Specifically, the activation of the CX3CR1 receptor by fractalkine induces the release of interleukin-1 beta from microglia, which modulates NMDA signaling in postsynaptic neurons, leading to the release of an eicosanoid messenger, which ultimately enhances presynaptic neurotransmitter release. In contrast to the conventional view, this form of plasticity does not require enhanced neuronal activity to trigger the events leading to synaptic facilitation. Augmentation of synaptic strength in nociceptive pathways represents a cellular model of pain amplification. The present data thus suggest that, under chronic pain states, CX3CR1-mediated activation of microglia drives the facilitation of excitatory synaptic transmission in the dorsal horn, which contributes to pain hypersensitivity in chronic pain states.
机译：认为突触可塑性仅由神经元引发，并且分配胶质细胞的普遍观点仅规定了突触传递和可塑性的支持功能。现在我们证明神经胶质细胞可以控制独立于神经元活动的突触强度。在这里，我们显示在大鼠中的小胶质细胞的选择性激活足以快速促进初级传入C纤维和椎板I神经元之间的突触强度，这是伤害感受途径中的第一个突触传递。具体而言，CX3CR1受体被fractalkine激活会诱导小胶质细胞释放白介素-1β，从而调节突触后神经元中的NMDA信号传导，从而导致类花生酸信使释放，最终增强突触前神经递质的释放。与传统观点相反，这种可塑性形式不需要增强神经元活动来触发导致突触促进的事件。伤害感受途径中突触强度的增强代表疼痛放大的细胞模型。因此，目前的数据表明，在慢性疼痛状态下，CX3CR1介导的小胶质细胞活化驱动背角兴奋性突触传递，这有助于慢性疼痛状态下的疼痛超敏反应。

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