神经病理性疼痛
突触后电位
神经科学
神经损伤
兴奋性突触后电位
神经传递
突触后密度
AMPA受体
医学
周围神经损伤
扣带回前部
谷氨酸受体
麻醉
抑制性突触后电位
心理学
内科学
坐骨神经
受体
认知
作者
Hui Xu,Long‐Jun Wu,Hansen Wang,Xuehan Zhang,Kunjumon I. Vadakkan,Susan S. Kim,Hendrik W. Steenland,Min Zhuo
标识
DOI:10.1523/jneurosci.1812-08.2008
摘要
Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.
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