nNOS-expressing neurons in the vmPFC transform pPVT-derived chronic pain signals into anxiety behaviors
nNOS-expressing neurons in the vmPFC transform pPVT-derived chronic pain signals into anxiety behaviors
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vmPFC 中表达 nNOS 的神经元将 pPVT 衍生的慢性疼痛信号转化为焦虑行为
DOI：
10.1038/s41467-020-16198-5
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发表时间：
2020-05-19
影响因子：
16.6
通讯作者：
Luo, Chun-Xia
中科院分区：
文献类型：
--
作者：
Liang, Hai-Ying;Chen, Zhi-Jin;Luo, Chun-Xia
Anxiety is common in patients suffering from chronic pain. Here, we report anxiety-like behaviors in mouse models of chronic pain and reveal that nNOS-expressing neurons in ventromedial prefrontal cortex (vmPFC) are essential for pain-induced anxiety but not algesia, using optogenetic and chemogenetic strategies. Additionally, we determined that excitatory projections from the posterior subregion of paraventricular thalamic nucleus (pPVT) provide a neuronal input that drives the activation of vmPFC nNOS-expressing neurons in our chronic pain models. Our results suggest that the pain signal becomes an anxiety signal after activation of vmPFC nNOS-expressing neurons, which causes subsequent release of nitric oxide (NO). Finally, we show that the downstream molecular mechanisms of NO likely involve enhanced glutamate transmission in vmPFC CaMKII alpha-expressing neurons through S-nitrosylation-induced AMPAR trafficking. Overall, our data suggest that pPVT excitatory neurons drive chronic pain-induced anxiety through activation of vmPFC nNOS-expressing neurons, resulting in NO-mediated AMPAR trafficking in vmPFC pyramidal neurons.
