4.7 Article

Electroacupuncture activates inhibitory neural circuits in the somatosensory cortex to relieve neuropathic pain

期刊

ISCIENCE
卷 24, 期 2, 页码 -

出版社

CELL PRESS
DOI: 10.1016/j.isci.2021.102066

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资金

  1. National Key Research and Development Program of China [2016YFC1306702]
  2. National Natural Science Foundation of China [81771455, 81971067, 32070955, 81973949]
  3. Outstanding Scholar Program of Guangzhou Regenerative Medicine and Health Guangdong Laboratory [2018GZR110102002]
  4. Science and Technology Program of Guangdong [2018B030334001]
  5. Science and Technology Program of Guangzhou, China [202007030012]
  6. Guangdong Natural Science Foundation [2019A1515011772]

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Using in vivo two-photon imaging, it was discovered that EA treatment can modulate the Ca2+ activity of neural circuits in the primary somatosensory cortex, leading to the suppression of excitatory pyramidal neurons and activation of specific interneurons. The alleviation of pain hypersensitivity and cortical modulation by EA is dependent on the activation of endocannabinoid receptor 1, revealing a molecular pathway for its analgesic effects.
Electroacupuncture (EA) has been accepted to effectively relieve neuropathic pain. Current knowledge of its neural modulation mainly covers the spinal cord and subcortical nuclei, with little evidence from the cortical regions. Using in vivo two-photon imaging in mice with chronic constriction injury, we found that EA treatment systemically modulated the Ca2+ activity of neural circuits in the primary somatosensory cortex, including the suppression of excitatory pyramidal neurons, potentiation of GABAergic somatostatin-positive interneurons, and suppression of vasoactive intestinal peptide-positive interneurons. Furthermore, EA-mediated alleviation of pain hypersensitivity and cortical modulation were dependent on the activation of endocannabinoid receptor 1. These findings collectively reveal a cortical circuit involved in relievingmechanical or thermal hypersensitivity under neuropathic pain and identify one molecular pathway directing analgesic effects of EA.

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