Involvement of basolateral amygdala-rostral anterior cingulate cortex in mechanical allodynia and anxiety-like behaviors and potential mechanisms of electroacupuncture

IF 4.8 1区 医学 Q1 NEUROSCIENCES CNS Neuroscience & Therapeutics Pub Date : 2024-09-15 DOI:10.1111/cns.70035
Yuerong Chen, Siyuan Tong, Yingling Xu, Yunyun Xu, Zonglin Wu, Xixiao Zhu, Xirui Wang, Chaoran Li, Chalian Lin, Xiaoyu Li, Chi Zhang, Yifang Wang, Xiaomei Shao, Jianqiao Fang, Yuanyuan Wu
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Abstract

Aims

Chronic pain is highly associated with anxiety. Electroacupuncture (EA) is effective in relieving pain and anxiety. Currently, little is known about the neural mechanisms underlying the comorbidity of chronic pain and anxiety and the EA mechanism. This study investigated a potential neural circuit underlying the comorbid and EA mechanisms.

Methods

Spared nerve injury (SNI) surgery established the chronic neuropathic pain mouse model. The neural circuit was activated or inhibited using the chemogenetic method to explore the relationship between the neural circuit and mechanical allodynia and anxiety-like behaviors. EA combined with the chemogenetic method was used to explore whether the effects of EA were related to this neural circuit.

Results

EA attenuated mechanical allodynia and anxiety-like behaviors in SNI mice, which may be associated with the activity of CaMKII neurons in the basolateral amygdala (BLA). Inhibition of BLACaMKII-rACC induced mechanical allodynia and anxiety-like behaviors in sham mice. Activation of the BLACaMKII-rACC alleviated neuropathic pain and anxiety-like behaviors in SNI mice. The analgesic and anxiolytic effects of 2 Hz EA were antagonized by the inhibition of the BLACaMKII-rACC.

Conclusion

BLACaMKII-rACC mediates mechanical allodynia and anxiety-like behaviors. The analgesic and anxiolytic effects of 2 Hz EA may be associated with the BLACaMKII-rACC.

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杏仁基底外侧-前扣带回皮层在机械异感和焦虑样行为中的参与以及电针的潜在机制
目的 慢性疼痛与焦虑密切相关。电针(EA)能有效缓解疼痛和焦虑。目前,人们对慢性疼痛和焦虑并存的神经机制以及 EA 机制知之甚少。本研究调查了一种潜在的神经回路,它是慢性疼痛和焦虑并存及 EA 机制的基础。 方法 裸神经损伤(SNI)手术建立了慢性神经病理性疼痛小鼠模型。利用化学遗传学方法激活或抑制神经回路,探讨神经回路与机械异感和焦虑样行为之间的关系。EA 与化学遗传学方法相结合,探讨 EA 的效应是否与该神经回路有关。 结果 EA减轻了SNI小鼠的机械异感和焦虑样行为,这可能与杏仁基底外侧(BLA)的CaMKII神经元的活性有关。抑制 BLACaMKII-rACC 可诱导假小鼠出现机械异感和焦虑样行为。激活 BLACaMKII-rACC 可减轻 SNI 小鼠的神经性疼痛和焦虑样行为。抑制 BLACaMKII-rACC 可拮抗 2 Hz EA 的镇痛和抗焦虑作用。 结论 BLACaMKII-rACC 介导机械异感和焦虑样行为。2 Hz EA 的镇痛和抗焦虑作用可能与 BLACaMKII-rACC 有关。
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来源期刊
CNS Neuroscience & Therapeutics
CNS Neuroscience & Therapeutics 医学-神经科学
CiteScore
7.30
自引率
12.70%
发文量
240
审稿时长
2 months
期刊介绍: CNS Neuroscience & Therapeutics provides a medium for rapid publication of original clinical, experimental, and translational research papers, timely reviews and reports of novel findings of therapeutic relevance to the central nervous system, as well as papers related to clinical pharmacology, drug development and novel methodologies for drug evaluation. The journal focuses on neurological and psychiatric diseases such as stroke, Parkinson’s disease, Alzheimer’s disease, depression, schizophrenia, epilepsy, and drug abuse.
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