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首页> 外文期刊>Neuron >The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain.
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The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain.

机译：AMPA受体亚基GluR-A和GluR-B相互调节脊髓突触可塑性和炎症性疼痛。

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摘要

Ca(2+)-permeable AMPA receptors are densely expressed in the spinal dorsal horn, but their functional significance in pain processing is not understood. By disrupting the genes encoding GluR-A or GluR-B, we generated mice exhibiting increased or decreased numbers of Ca(2+)-permeable AMPA receptors, respectively. Here, we demonstrate that AMPA receptors are critical determinants of nociceptive plasticity and inflammatory pain. A reduction in the number of Ca(2+)-permeable AMPA receptors and density of AMPA channel currents in spinal neurons of GluR-A-deficient mice is accompanied by a loss of nociceptive plasticity in vitro and a reduction in acute inflammatory hyperalgesia in vivo. In contrast, an increase in spinal Ca(2+)-permeable AMPA receptors in GluR-B-deficient mice facilitated nociceptive plasticity and enhanced long-lasting inflammatory hyperalgesia. Thus, AMPA receptors are not mere determinants of fast synaptic transmission underlying basal pain sensitivity as previously thought, but are critically involved in activity-dependent changes in synaptic processing of nociceptive inputs.
机译：Ca（2+）渗透性AMPA受体在脊髓背角中密集表达，但它们在疼痛处理中的功能意义尚不明确。通过破坏编码GluR-A或GluR-B的基因，我们生成了分别表现出增加或减少的Ca（2+）渗透性AMPA受体数量的小鼠。在这里，我们证明AMPA受体是伤害性可塑性和炎性疼痛的关键决定因素。 Ca（2+）渗透性AMPA受体数量的减少和GluR-A缺陷小鼠脊髓神经元中AMPA通道电流的密度伴随着体外伤害感受可塑性的丧失和体内急性炎性痛觉过敏的减少。相反，在GluR-B缺陷型小鼠中，脊髓Ca（2+）渗透性AMPA受体的增加促进了伤害性可塑性并增强了持久性炎性痛觉过敏。因此，AMPA受体不仅是先前认为的基础疼痛敏感性基础上的快速突触传递的决定因素，而且还与伤害性输入的突触加工过程中的活性依赖变化密切相关。

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