Increased spinal cord Na⁺-K⁺-2Cl⁻ cotransporter-1 (NKCC1) activity contributes to impairment of synaptic inhibition in paclitaxel-induced neuropathic pain.
摘要：Background: Spinal synaptic plasticity may contribute to paclitaxel-induced painful neuropathy.
Results: Paclitaxel treatment impairs GABA-mediated neuronal inhibition and increases total and plasma membrane NKCC1
protein levels in the spinal cord. Blocking NKCC1 reverses paclitaxel effects on synaptic inhibition and pain hypersensitivity.
Conclusion: Paclitaxel diminishes synaptic inhibition in the spinal cord.
Significance: This study demonstrates how disrupting microtubule dynamics causes synaptic plasticity and neuropathic
pain.
关键词：生理学
论文方向：[{"id":15,"name":"生理学"}]
发表期刊：The American Society for Biochemistry and Molecular Biology
数字识别码：jbc.M114.600320
是否作者本人： 是
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