A sleep-active basalocortical pathway crucial for generation and maintenance of chronic pain.

A sleep-active basalocortical pathway crucial for generation and maintenance of chronic pain.
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睡眠活跃的基底层途径对于慢性疼痛的产生和维持至关重要。

DOI:
10.1038/s41593-022-01250-y
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发表时间:
2023-03
影响因子:
25
通讯作者:
Yang, Guang
Yang, Guang
中科院分区:
医学1区
文献类型:
--
作者:
Zhou, Hang;Li, Miao;Zhao, Ruohe;Sun, Linlin;Yang, Guang

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Poor sleep is associated with the risk of developing chronic pain, but how sleep contributes to pain chronicity remains unclear. Here we show that following peripheral nerve injury, cholinergic neurons in the anterior nucleus basalis (aNB) of the basal forebrain are increasingly active during non-rapid eye movement (NREM) sleep in a mouse model of neuropathic pain. These neurons directly activate vasoactive intestinal polypeptide-expressing interneurons in the primary somatosensory cortex (S1), causing disinhibition of pyramidal neurons and allodynia. The hyperactivity of aNB neurons is caused by the increased inputs from the parabrachial nucleus (PB) driven by the injured peripheral afferents. Inhibition of this pathway during NREM sleep, but not wakefulness, corrects neuronal hyperactivation and alleviates pain. Our results reveal that the PB–aNB–S1 pathway during sleep is critical for the generation and maintenance of chronic pain. Inhibiting this pathway during the sleep phase could be important for treating neuropathic pain.
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