nNOS-expressing neurons in the vmPFC transform pPVT-derived chronic pain signals into anxiety behaviors

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 chemogenet...

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Published inNature communications Vol. 11; no. 1; pp. 2501 - 18
Main Authors Liang, Hai-Ying, Chen, Zhi-Jin, Xiao, Hui, Lin, Yu-Hui, Hu, Ying-Yi, Chang, Lei, Wu, Hai-Yin, Wang, Peng, Lu, Wei, Zhu, Dong-Ya, Luo, Chun-Xia
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 19.05.2020
Nature Publishing Group
Nature Portfolio
Subjects
13/51
13/89
14/19
14/32
631/378
64/110
64/60
692/699
9/74
Activation
Animal models
Animals
Anxiety
Behavior, Animal
Chronic pain
Chronic Pain - enzymology
Chronic Pain - genetics
Chronic Pain - psychology
Humanities and Social Sciences
Humans
Male
Mice
Mice, Inbred C57BL
Midline Thalamic Nuclei - cytology
Midline Thalamic Nuclei - enzymology
Molecular modelling
multidisciplinary
Neurons
Neurons - cytology
Neurons - enzymology
Nitric oxide
Nitric Oxide - metabolism
Nitric Oxide Synthase Type I - genetics
Nitric Oxide Synthase Type I - metabolism
Pain
Prefrontal cortex
Prefrontal Cortex - cytology
Prefrontal Cortex - enzymology
Pyramidal cells
Science
Science (multidisciplinary)
Thalamus
α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors
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Abstract 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 CaMKIIα-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. Chronic pain usually induces anxiety. Here, the authors report that vmPFC nNOS-expressing neurons are activated by excitatory inputs from pPVT during chronic pain and subsequently induce anxiety-like behaviors in mice through promoting AMPAR trafficking.
AbstractList 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 CaMKIIα-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.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 CaMKIIα-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.
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 CaMKIIα-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.Chronic pain usually induces anxiety. Here, the authors report that vmPFC nNOS-expressing neurons are activated by excitatory inputs from pPVT during chronic pain and subsequently induce anxiety-like behaviors in mice through promoting AMPAR trafficking.
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 CaMKIIα-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. Chronic pain usually induces anxiety. Here, the authors report that vmPFC nNOS-expressing neurons are activated by excitatory inputs from pPVT during chronic pain and subsequently induce anxiety-like behaviors in mice through promoting AMPAR trafficking.
Chronic pain usually induces anxiety. Here, the authors report that vmPFC nNOS-expressing neurons are activated by excitatory inputs from pPVT during chronic pain and subsequently induce anxiety-like behaviors in mice through promoting AMPAR trafficking.
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 CaMKIIα-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.
ArticleNumber 2501
Author Wang, Peng
Lu, Wei
Hu, Ying-Yi
Chang, Lei
Zhu, Dong-Ya
Luo, Chun-Xia
Chen, Zhi-Jin
Wu, Hai-Yin
Xiao, Hui
Lin, Yu-Hui
Liang, Hai-Ying
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32427844$$D View this record in MEDLINE/PubMed
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Snippet Anxiety is common in patients suffering from chronic pain. Here, we report anxiety-like behaviors in mouse models of chronic pain and reveal that...
Chronic pain usually induces anxiety. Here, the authors report that vmPFC nNOS-expressing neurons are activated by excitatory inputs from pPVT during chronic...
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pubmedcentral
proquest
pubmed
crossref
springer
SourceType Open Website
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StartPage 2501
SubjectTerms 13/51
13/89
14/19
14/32
631/378
64/110
64/60
692/699
9/74
Activation
Animal models
Animals
Anxiety
Behavior, Animal
Chronic pain
Chronic Pain - enzymology
Chronic Pain - genetics
Chronic Pain - psychology
Humanities and Social Sciences
Humans
Male
Mice
Mice, Inbred C57BL
Midline Thalamic Nuclei - cytology
Midline Thalamic Nuclei - enzymology
Molecular modelling
multidisciplinary
Neurons
Neurons - cytology
Neurons - enzymology
Nitric oxide
Nitric Oxide - metabolism
Nitric Oxide Synthase Type I - genetics
Nitric Oxide Synthase Type I - metabolism
Pain
Prefrontal cortex
Prefrontal Cortex - cytology
Prefrontal Cortex - enzymology
Pyramidal cells
Science
Science (multidisciplinary)
Thalamus
α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors
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Title nNOS-expressing neurons in the vmPFC transform pPVT-derived chronic pain signals into anxiety behaviors
URI https://link.springer.com/article/10.1038/s41467-020-16198-5
https://www.ncbi.nlm.nih.gov/pubmed/32427844
https://www.proquest.com/docview/2404627792
https://www.proquest.com/docview/2405307845
https://pubmed.ncbi.nlm.nih.gov/PMC7237711
https://doaj.org/article/8f56e6d3aab84052a130814cd8153048
Volume 11
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