Paraventricular nucleus‐central amygdala oxytocinergic projection modulates pain‐related anxiety‐like behaviors in mice

Anxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the role of paraventricular nucleus (PVN)-central nucleus of the amygdala (CeA) oxytocinergic projections in anxiety-like behaviors induced by infl...

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Published inCNS neuroscience & therapeutics Vol. 29; no. 11; pp. 3493 - 3506
Main Authors Li, Yu‐Jie, Du, Wei‐Jia, Liu, Rui, Zan, Gui‐Ying, Ye, Bing‐Lu, Li, Qian, Sheng, Zhi‐Hao, Yuan, Ya‐Wei, Song, Yu‐Jie, Liu, Jing‐Gen, Liu, Zhi‐Qiang
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Published England John Wiley & Sons, Inc 01.11.2023
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Abstract Anxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the role of paraventricular nucleus (PVN)-central nucleus of the amygdala (CeA) oxytocinergic projections in anxiety-like behaviors induced by inflammatory pain. After inflammatory pain induction by complete Freund's adjuvant (CFA), mice underwent elevated plus maze, light-dark transition test, and marble burying test to examine the anxiety-like behaviors. Chemogenetic, optogenetic, and fiber photometry recordings were used to modulate and record the activity of the oxytocinergic projections of the PVN-CeA. The key results are as follows: inflammatory pain-induced anxiety-like behaviors in mice accompanied by decreased activity of PVN oxytocin neurons. Chemogenetic activation of PVN oxytocin neurons prevented pain-related anxiety-like behaviors, whereas inhibition of PVN oxytocin neurons induced anxiety-like behaviors in naïve mice. PVN oxytocin neurons projected directly to the CeA, and microinjection of oxytocin into the CeA blocked anxiety-like behaviors. Inflammatory pain also decreased the activity of CeA neurons, and optogenetic activation of PVN -CeA circuit prevented anxiety-like behavior in response to inflammatory pain. The results of our study suggest that oxytocin has anti-anxiety effects and provide novel insights into the role of PVN -CeA projections in the regulation of anxiety-like behaviors induced by inflammatory pain.
AbstractList Anxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the role of paraventricular nucleus (PVN)-central nucleus of the amygdala (CeA) oxytocinergic projections in anxiety-like behaviors induced by inflammatory pain.AIMSAnxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the role of paraventricular nucleus (PVN)-central nucleus of the amygdala (CeA) oxytocinergic projections in anxiety-like behaviors induced by inflammatory pain.After inflammatory pain induction by complete Freund's adjuvant (CFA), mice underwent elevated plus maze, light-dark transition test, and marble burying test to examine the anxiety-like behaviors. Chemogenetic, optogenetic, and fiber photometry recordings were used to modulate and record the activity of the oxytocinergic projections of the PVN-CeA.METHODSAfter inflammatory pain induction by complete Freund's adjuvant (CFA), mice underwent elevated plus maze, light-dark transition test, and marble burying test to examine the anxiety-like behaviors. Chemogenetic, optogenetic, and fiber photometry recordings were used to modulate and record the activity of the oxytocinergic projections of the PVN-CeA.The key results are as follows: inflammatory pain-induced anxiety-like behaviors in mice accompanied by decreased activity of PVN oxytocin neurons. Chemogenetic activation of PVN oxytocin neurons prevented pain-related anxiety-like behaviors, whereas inhibition of PVN oxytocin neurons induced anxiety-like behaviors in naïve mice. PVN oxytocin neurons projected directly to the CeA, and microinjection of oxytocin into the CeA blocked anxiety-like behaviors. Inflammatory pain also decreased the activity of CeA neurons, and optogenetic activation of PVNoxytocin -CeA circuit prevented anxiety-like behavior in response to inflammatory pain.RESULTSThe key results are as follows: inflammatory pain-induced anxiety-like behaviors in mice accompanied by decreased activity of PVN oxytocin neurons. Chemogenetic activation of PVN oxytocin neurons prevented pain-related anxiety-like behaviors, whereas inhibition of PVN oxytocin neurons induced anxiety-like behaviors in naïve mice. PVN oxytocin neurons projected directly to the CeA, and microinjection of oxytocin into the CeA blocked anxiety-like behaviors. Inflammatory pain also decreased the activity of CeA neurons, and optogenetic activation of PVNoxytocin -CeA circuit prevented anxiety-like behavior in response to inflammatory pain.The results of our study suggest that oxytocin has anti-anxiety effects and provide novel insights into the role of PVNoxytocin -CeA projections in the regulation of anxiety-like behaviors induced by inflammatory pain.CONCLUSIONThe results of our study suggest that oxytocin has anti-anxiety effects and provide novel insights into the role of PVNoxytocin -CeA projections in the regulation of anxiety-like behaviors induced by inflammatory pain.
Anxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the role of paraventricular nucleus (PVN)-central nucleus of the amygdala (CeA) oxytocinergic projections in anxiety-like behaviors induced by inflammatory pain. After inflammatory pain induction by complete Freund's adjuvant (CFA), mice underwent elevated plus maze, light-dark transition test, and marble burying test to examine the anxiety-like behaviors. Chemogenetic, optogenetic, and fiber photometry recordings were used to modulate and record the activity of the oxytocinergic projections of the PVN-CeA. The key results are as follows: inflammatory pain-induced anxiety-like behaviors in mice accompanied by decreased activity of PVN oxytocin neurons. Chemogenetic activation of PVN oxytocin neurons prevented pain-related anxiety-like behaviors, whereas inhibition of PVN oxytocin neurons induced anxiety-like behaviors in naïve mice. PVN oxytocin neurons projected directly to the CeA, and microinjection of oxytocin into the CeA blocked anxiety-like behaviors. Inflammatory pain also decreased the activity of CeA neurons, and optogenetic activation of PVN -CeA circuit prevented anxiety-like behavior in response to inflammatory pain. The results of our study suggest that oxytocin has anti-anxiety effects and provide novel insights into the role of PVN -CeA projections in the regulation of anxiety-like behaviors induced by inflammatory pain.
Our study suggests that oxytocin has anti‐anxiety effects and provides novel insights into the role of PVN‐CeA oxytocin projections in the regulation of anxiety‐like behaviors induced by inflammatory pain.
AimsAnxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the role of paraventricular nucleus (PVN)-central nucleus of the amygdala (CeA) oxytocinergic projections in anxiety-like behaviors induced by inflammatory pain.MethodsAfter inflammatory pain induction by complete Freund's adjuvant (CFA), mice underwent elevated plus maze, light–dark transition test, and marble burying test to examine the anxiety-like behaviors. Chemogenetic, optogenetic, and fiber photometry recordings were used to modulate and record the activity of the oxytocinergic projections of the PVN-CeA.ResultsThe key results are as follows: inflammatory pain-induced anxiety-like behaviors in mice accompanied by decreased activity of PVN oxytocin neurons. Chemogenetic activation of PVN oxytocin neurons prevented pain-related anxiety-like behaviors, whereas inhibition of PVN oxytocin neurons induced anxiety-like behaviors in naïve mice. PVN oxytocin neurons projected directly to the CeA, and microinjection of oxytocin into the CeA blocked anxiety-like behaviors. Inflammatory pain also decreased the activity of CeA neurons, and optogenetic activation of PVNoxytocin-CeA circuit prevented anxiety-like behavior in response to inflammatory pain.ConclusionThe results of our study suggest that oxytocin has anti-anxiety effects and provide novel insights into the role of PVNoxytocin-CeA projections in the regulation of anxiety-like behaviors induced by inflammatory pain.
Author Liu, Rui
Li, Qian
Sheng, Zhi‐Hao
Song, Yu‐Jie
Liu, Zhi‐Qiang
Du, Wei‐Jia
Ye, Bing‐Lu
Yuan, Ya‐Wei
Liu, Jing‐Gen
Li, Yu‐Jie
Zan, Gui‐Ying
AuthorAffiliation 2 Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica Chinese Academy of Sciences Shanghai China
1 Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal‐Fetal Medicine and Gynecologic Oncology, Department of Anesthesiology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Medicine Tongji University Shanghai China
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Issue 11
Keywords anxiety
oxytocin
pain
central nucleus of the amygdala
paraventricular nucleus
Language English
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Snippet Anxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate the...
AimsAnxiety disorders associated with pain are a common health problem. However, the underlying mechanisms remain poorly understood. We aimed to investigate...
Our study suggests that oxytocin has anti‐anxiety effects and provides novel insights into the role of PVN‐CeA oxytocin projections in the regulation of...
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StartPage 3493
SubjectTerms Amygdala
Animal behavior
Anxiety
Anxiety disorders
Brain
Emotions
Freund's adjuvant
Hormones
Inflammation
Laboratory animals
Life sciences
Microinjection
Neurons
Original
Oxytocin
Pain
Paraventricular nucleus
Photometry
Video recorders
Title Paraventricular nucleus‐central amygdala oxytocinergic projection modulates pain‐related anxiety‐like behaviors in mice
URI https://www.ncbi.nlm.nih.gov/pubmed/37248645
https://www.proquest.com/docview/2877674946
https://www.proquest.com/docview/2820967870
https://pubmed.ncbi.nlm.nih.gov/PMC10580334
Volume 29
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