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Editor | Xi epidemiological studies show that more than 50% of chronic pain patients are accompanied by depression, and more than 60% of depression patients are accompanied by physical pain.
Once pain and depression are comorbid, a vicious circle can easily develop into a refractory disease (insensitive to drug treatment).
The huge challenge is that the neural mechanism of its pathogenesis is not yet clear, and it has always been a difficult point in clinical treatment.
Zhang Zhi's research group from the Department of Life Sciences and Medicine, University of Science and Technology of China has long been committed to the study of the neural mechanism of the interaction between pain and emotion.
The previous research has analyzed the subcortical neural circuit mechanism of chronic pain leading to depression (Nature Neuroscience, 2019).
Physical intervention in specific brain regions or neural circuits is a hot spot for current treatment of neurological diseases that are not sensitive to drugs, such as repetitive transcranial magnetic stimulation (rTMS) and deep brain stimulation.
Different intervention methods have their own advantages and disadvantages.
Taking rTMS as an example, it is non-invasive and has low side effects, but requires high accuracy of the intervention target, and the effective depth of intervention is only limited to the cortex.
The research team and clinical collaborative research found that rTMS intervention in the specific cortex of patients with obsessive-compulsive disorder can relieve symptoms (PNAS, 2019).
Therefore, the research team further analyzed the cortical neural circuit basis of the interaction between pain and emotion on the basis of the past.
On March 8, 2021, Zhang Zhi’s group and Li Juan’s team from the Department of Anesthesiology, The First Affiliated Hospital of China University of Science and Technology (Anhui Provincial Hospital) jointly published an article on Nature Neuroscience "Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression -like states", found that the body pain caused by depression and the pain caused by tissue damage have a different thalamic-cortical neural circuit basis.
The thalamus is a relay station for the transmission of pain information.
It gathers and integrates pain signals from nuclei such as the spinal cord and brainstem, and finally differentiates and fine-processes pain information through the thalamus-cortex connection.
The study used mouse plantar inflammation and nerve ligation as a tissue injury pain model, combined with virus tracing, in vivo multi-channel/fiber recording, and two-photon calcium imaging.
It was found that the posterior thalamic nucleus (PO) projects to the primary sensation.
The neural circuit (POGlu→S1Glu) of the cortex (S1) is involved in the hyperalgesia caused by tissue damage.
In addition, mice that produce depression-like behaviors under chronic stress also exhibit hyperalgesia (as an animal model for physical pain in patients with depression).
Interestingly, in this model animal, regulating the activity of the POGlu→S1Glu neural circuit did not affect the hyperalgesic behavior, but it was found that the parafascicular nucleus (PF) of the thalamus projected to the anterior cingulate cortex (ACC) neural circuit (PFGlu).
→ACCGABA→Glu) is involved in the hyperalgesia of depression.
This research not only provides in-depth and new theoretical insights into the pathogenesis of physical pain caused by different causes (clinical treatment plans and therapeutic effects are not the same), but also may be used for clinical use of rTMS and other precise targeting of specific neural circuits.
Physical intervention therapy provides new strategies.
Tissue injury and depression produce painful thalamus-cortical neural circuit pattern diagram, Chinese University of Science and Technology of Life Sciences and Medical Sciences students Tang Haodi and Dong Wanying, and the Chinese University of Science and Technology of the First Affiliated Hospital of Postdoctoral Department of Anesthesiology Zhu Xia and Director Kang Fang are the co-first authors, Zhang Zhi, Juan Li and Jin Yan are the co-corresponding authors.
The research collaborators included Xue Tian, Song Xiaoyuan, and Zhang Yan from the University of Science and Technology of China (with the Department of Neurology of the First Hospital), as well as directors Zhang Xulai and Xie Wen of the Fourth People's Hospital of Hefei.
Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Reprinting is prohibited without permission.
The author has all legal rights and offenders must be investigated.
Original link https://dx.
doi.
org/10.
1038/s41593-021-00811-x Plate maker: Qi Jiang
Once pain and depression are comorbid, a vicious circle can easily develop into a refractory disease (insensitive to drug treatment).
The huge challenge is that the neural mechanism of its pathogenesis is not yet clear, and it has always been a difficult point in clinical treatment.
Zhang Zhi's research group from the Department of Life Sciences and Medicine, University of Science and Technology of China has long been committed to the study of the neural mechanism of the interaction between pain and emotion.
The previous research has analyzed the subcortical neural circuit mechanism of chronic pain leading to depression (Nature Neuroscience, 2019).
Physical intervention in specific brain regions or neural circuits is a hot spot for current treatment of neurological diseases that are not sensitive to drugs, such as repetitive transcranial magnetic stimulation (rTMS) and deep brain stimulation.
Different intervention methods have their own advantages and disadvantages.
Taking rTMS as an example, it is non-invasive and has low side effects, but requires high accuracy of the intervention target, and the effective depth of intervention is only limited to the cortex.
The research team and clinical collaborative research found that rTMS intervention in the specific cortex of patients with obsessive-compulsive disorder can relieve symptoms (PNAS, 2019).
Therefore, the research team further analyzed the cortical neural circuit basis of the interaction between pain and emotion on the basis of the past.
On March 8, 2021, Zhang Zhi’s group and Li Juan’s team from the Department of Anesthesiology, The First Affiliated Hospital of China University of Science and Technology (Anhui Provincial Hospital) jointly published an article on Nature Neuroscience "Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression -like states", found that the body pain caused by depression and the pain caused by tissue damage have a different thalamic-cortical neural circuit basis.
The thalamus is a relay station for the transmission of pain information.
It gathers and integrates pain signals from nuclei such as the spinal cord and brainstem, and finally differentiates and fine-processes pain information through the thalamus-cortex connection.
The study used mouse plantar inflammation and nerve ligation as a tissue injury pain model, combined with virus tracing, in vivo multi-channel/fiber recording, and two-photon calcium imaging.
It was found that the posterior thalamic nucleus (PO) projects to the primary sensation.
The neural circuit (POGlu→S1Glu) of the cortex (S1) is involved in the hyperalgesia caused by tissue damage.
In addition, mice that produce depression-like behaviors under chronic stress also exhibit hyperalgesia (as an animal model for physical pain in patients with depression).
Interestingly, in this model animal, regulating the activity of the POGlu→S1Glu neural circuit did not affect the hyperalgesic behavior, but it was found that the parafascicular nucleus (PF) of the thalamus projected to the anterior cingulate cortex (ACC) neural circuit (PFGlu).
→ACCGABA→Glu) is involved in the hyperalgesia of depression.
This research not only provides in-depth and new theoretical insights into the pathogenesis of physical pain caused by different causes (clinical treatment plans and therapeutic effects are not the same), but also may be used for clinical use of rTMS and other precise targeting of specific neural circuits.
Physical intervention therapy provides new strategies.
Tissue injury and depression produce painful thalamus-cortical neural circuit pattern diagram, Chinese University of Science and Technology of Life Sciences and Medical Sciences students Tang Haodi and Dong Wanying, and the Chinese University of Science and Technology of the First Affiliated Hospital of Postdoctoral Department of Anesthesiology Zhu Xia and Director Kang Fang are the co-first authors, Zhang Zhi, Juan Li and Jin Yan are the co-corresponding authors.
The research collaborators included Xue Tian, Song Xiaoyuan, and Zhang Yan from the University of Science and Technology of China (with the Department of Neurology of the First Hospital), as well as directors Zhang Xulai and Xie Wen of the Fourth People's Hospital of Hefei.
Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Reprinting is prohibited without permission.
The author has all legal rights and offenders must be investigated.
Original link https://dx.
doi.
org/10.
1038/s41593-021-00811-x Plate maker: Qi Jiang
