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Inhibitory gamma-aminobutyric acidergic neurons in the anterior cingulate cortex participate in the comorbidity of pain and emotion

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Neural Regeneration Research 2025年第10期20卷 2838-2854页

作者： Lu Guan Mengting Qiu Na Li Zhengxiang Zhou Ru Ye Liyan Zhong Yashuang Xu Junhui Ren Yi Liang Xiaomei Shao Jianqiao Fang Junfan Fang Junying Du Department of Neurobiology and Acupuncture Research Third School of Clinical MedicineZhejiang Chinese Medical UniversityHangzhouZhejiang ProvinceChina Key Laboratory for Research of Acupuncture Treatment and Transformation of Emotional Diseases Third School of Clinical MedicineZhejiang Chinese Medical UniversityHangzhouZhejiang ProvinceChina Fuchun Community Health Service Center of Fuyang District HangzhouZhejiang ProvinceChina

Pain is often comorbid with emotional disorders such as anxiety and *** of the anterior cingulate cortex has been implicated in pain and pain-related negative emotions that arise from impairments in inhibitory gamma-aminobutyric acid *** review primarily aims to outline the main circuitry(including the input and output connectivity)of the anterior cingulate cortex and classification and functions of different gamma-aminobutyric acidergic neurons;it also describes the neurotransmitters/neuromodulators affecting these neurons,their intercommunication with other neurons,and their importance in mental comorbidities associated with chronic pain *** understanding on their role in pain-related mental comorbidities may facilitate the development of more effective treatments for these ***,the mechanisms that regulate gamma-aminobutyric acidergic systems remain *** is also unclear as to whether the mechanisms are presynaptic or *** exploration of the complexities of this system may reveal new pathways for research and drug development.

关键词： anterior cingulate cortex anxiety chronic pain circuit communication comorbidity depression gamma-aminobutyric acidergic neurons parvalbumin neurons synaptic transmission

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An inhibitory nigra-parafascicular pathway mediates the development of temporal lobe epilepsy

An inhibitory nigra-parafascicular pathway mediates the deve...

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中国神经科学学会第十二届全国学术会议

作者： Bin Chena Ying Wanga Cenglin Xua Yi Wang Heming Cheng Liying Chen Tingting Hu Junli Zhao Zhong Chen Department of Pharmacology Key Laboratory of Medical Neurobiology of the Ministry of Health of China School of Basic Medical Sciences College of Pharmaceutical Sciences Zhejiang University Epilepsy Center Second Affiliated Hospital School of Medicine Zhejiang University Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases First Affiliated Hospital School of Medicine Zhejiang University

The substantia nigra pars reticulata（SNr）, a region that mainly contains GABAergic neurons, is thought to be involved in epilepsy, but its precise cellular and neuronal circuitry mechanisms in temporal lobe epilepsy（TLE） have not been investigated. Using single-unit recordings and calcium fiber photometry, we found that SNr GABAergic/parvalbumin（PV） neurons were activated during seizures. Optogenetic and chemogenetic inhibition of SNr PV neurons retarded the development of TLE, whereas activation of these neurons promoted the development of TLE. In addition, epilepsy was bilaterally regulated by optogenetic manipulation of SNr PV projection fibers in the parafascicular nucleus（PF）, but not in the reticularis nucleus（RT） or the reuniens nucleus（RE）. Furthermore, in vivo/in vitro electrophysiology combined with rabies virus-assisted circuit-mapping, showed that SNr PV neurons directly project to PF GABAergic neurons. Finally, optogenetic manipulation of PF GABAergic neurons mimicked the role of PF-projecting PV fibers from the SNr in the development of TLE. Optogenetic activation of PF GABAergic neurons retarded the development of TLE, whereas inhibition of these neurons promoted the development of TLE. Collectively, our results revealed a previously unknown neural pathway, originating from SNr PV neurons to PF GABAergic neurons, involved in TLE. These findings are relevant for a better understanding of pathological network changes and might provide new insight for therapeutic manipulations in TLE.

关键词： temporal lobe epilepsy inhibitory neuronal circuit parvalbumin neurons substantia nigra pars reticulata parafascicular nucleus

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