Activation of VIP interneurons in the prefrontal cortex ameliorates neuropathic pain aversiveness.
Activation of VIP interneurons in the prefrontal cortex ameliorates neuropathic pain aversiveness.
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DOI：
10.1016/j.celrep.2022.111333
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发表时间：
2022-09-13
期刊：
影响因子：
8.8
通讯作者：
Yang, Guang
中科院分区：
文献类型：
--
作者：
Li, Miao;Zhou, Hang;Teng, Sasa;Yang, Guang
While dysfunction of the medial prefrontal cortex (mPFC) has been implicated in chronic pain, the underlying neural circuits and the contribution of specific cellular populations remain unclear. Using in vivo Ca2+ imaging, we report that in both male and female mice, peripheral nerve injury-induced neuropathic pain causes a marked reduction of vasoactive intestinal polypeptide (VIP)-expressing interneuron activity in the prelimbic area of the mPFC, which contributes to decreased prefrontal cortical outputs. Moreover, prelimbic glutamatergic projections to GABAergic interneurons in the anterior cingulate cortex (ACC) are diminished, leading to loss of cortical-cortical inhibition and increased pyramidal neuron activity in the ACC. Chemogenetic activation of prelimbic VIP interneurons restores neuronal responses in the mPFC-ACC pathway and attenuates pain-like behaviors in mice. Furthermore, restoration of prelimbic outputs to the ACC reverses nerve injury-induced ACC hyperactivation. These findings reveal mPFC circuit changes associated with neuropathic pain and highlight VIP interneurons as potential therapeutic targets for pain treatment. Vasoactive intestinal polypeptide (VIP)-expressing interneurons provide disinhibitory control of cortical circuits. Li et al. show that neuropathic pain reduces VIP neuronal activity in the mouse prefrontal cortex. Chemogenetic activation of VIP interneurons restores prefrontal outputs to the anterior cingulate cortex and ameliorates pain-like behaviors in mice.
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