Long-term potentiation in the anterior cingulate cortex and chronic pain.

Long-term potentiation in the anterior cingulate cortex and chronic pain.
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DOI:
10.1098/rstb.2013.0146
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发表时间:
2014-01-05
期刊:
Philosophical transactions of the Royal Society of London. Series B, Biological sciences
影响因子:
--
通讯作者:
Zhuo M
Zhuo M
中科院分区:
其他
文献类型:
--
作者:
Zhuo M

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谷氨酸是中枢神经系统中感觉传递和感知的主要兴奋性递质。来自外周的疼痛或有害刺激“教导”人类和动物避免潜在危险的物体或环境,而组织损伤本身会导致不必要的慢性疼痛,甚至可能持续很长一段时间。传统的止痛药往往无法控制慢性疼痛。最近的神经生物学研究表明,从脊髓背角到皮层区域的感觉通路中发生的突触可塑性有助于慢性疼痛。损伤触发脊髓背角和前扣带皮层中突触传递的长时程增强,并且这种持续增强不需要来自外周的连续神经元活动。在突触水平,损伤引起的兴奋性传递增强可能是通过突触前末梢谷氨酸释放的增强和AMPA受体突触后反应的增强来介导的。预防、“消除”或减少这种增强作用可能会成为未来抑制患者慢性疼痛的新机制。
Glutamate is the primary excitatory transmitter of sensory transmission and perception in the central nervous system. Painful or noxious stimuli from the periphery ‘teach’ humans and animals to avoid potentially dangerous objects or environments, whereas tissue injury itself causes unnecessary chronic pain that can even last for long periods of time. Conventional pain medicines often fail to control chronic pain. Recent neurobiological studies suggest that synaptic plasticity taking place in sensory pathways, from spinal dorsal horn to cortical areas, contributes to chronic pain. Injuries trigger long-term potentiation of synaptic transmission in the spinal cord dorsal horn and anterior cingulate cortex, and such persistent potentiation does not require continuous neuronal activity from the periphery. At the synaptic level, potentiation of excitatory transmission caused by injuries may be mediated by the enhancement of glutamate release from presynaptic terminals and potentiated postsynaptic responses of AMPA receptors. Preventing, ‘erasing’ or reducing such potentiation may serve as a new mechanism to inhibit chronic pain in patients in the future.
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