Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease
Abstract Parkinson’s disease (PD) is a multi-system neurodegenerative disorder. Patients with PD often suffer chronic pain. In the present study, we investigated motor, sensory and emotional changes in three different PD mice models. We found that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-...
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oai:doaj.org-article:8d3f98e132d14b2b9478cacc6a82f1e62021-11-08T11:17:11ZSynaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease10.1186/s13041-021-00870-y1756-6606https://doaj.org/article/8d3f98e132d14b2b9478cacc6a82f1e62021-11-01T00:00:00Zhttps://doi.org/10.1186/s13041-021-00870-yhttps://doaj.org/toc/1756-6606Abstract Parkinson’s disease (PD) is a multi-system neurodegenerative disorder. Patients with PD often suffer chronic pain. In the present study, we investigated motor, sensory and emotional changes in three different PD mice models. We found that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treatment caused significant changes in all measurements. Mechanical hypersensitivity of PD model induced by MPTP peaked at 3 days and persisted for at least 14 days. Using Fos transgenic mice, we found that neurons in the anterior cingulate cortex (ACC) were activated after MPTP treatment. Inhibiting ACC by bilateral microinjection of muscimol significantly reduced mechanical hypersensitivity and anxiety-like responses. By contrast, MPTP induced motor deficit was not affected, indicating ACC activity is mostly responsible for sensory and emotional changes. We also investigated excitatory synaptic transmission and plasticity using brain slices of MPTP treated animals. While L-LTP was blocked or significantly reduced. E-LTP was not significantly affected in slices of MPTP treated animals. LTD induced by repetitive stimulation was not affected. Furthermore, we found that paired-pulse facilitation and spontaneous release of glutamate were also altered in MPTP treated animals, suggesting presynaptic enhancement of excitatory transmission in PD. Our results suggest that ACC synaptic transmission is enhanced in the animal model of PD, and cortical excitation may play important roles in PD related pain and anxiety.Zhaoxiang ZhouPenghai YeXu-Hui LiYuxiang ZhangMuhang LiQi-Yu ChenJing-Shan LuMan XueYanan LiWeiqi LiuLin LuWantong ShiPing-Yi XuMin ZhuoBMCarticleParkinson’s diseaseChronic painACCLTPMPTPNeurology. Diseases of the nervous systemRC346-429ENMolecular Brain, Vol 14, Iss 1, Pp 1-17 (2021) |
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Parkinson’s disease Chronic pain ACC LTP MPTP Neurology. Diseases of the nervous system RC346-429 |
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Parkinson’s disease Chronic pain ACC LTP MPTP Neurology. Diseases of the nervous system RC346-429 Zhaoxiang Zhou Penghai Ye Xu-Hui Li Yuxiang Zhang Muhang Li Qi-Yu Chen Jing-Shan Lu Man Xue Yanan Li Weiqi Liu Lin Lu Wantong Shi Ping-Yi Xu Min Zhuo Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease |
description |
Abstract Parkinson’s disease (PD) is a multi-system neurodegenerative disorder. Patients with PD often suffer chronic pain. In the present study, we investigated motor, sensory and emotional changes in three different PD mice models. We found that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treatment caused significant changes in all measurements. Mechanical hypersensitivity of PD model induced by MPTP peaked at 3 days and persisted for at least 14 days. Using Fos transgenic mice, we found that neurons in the anterior cingulate cortex (ACC) were activated after MPTP treatment. Inhibiting ACC by bilateral microinjection of muscimol significantly reduced mechanical hypersensitivity and anxiety-like responses. By contrast, MPTP induced motor deficit was not affected, indicating ACC activity is mostly responsible for sensory and emotional changes. We also investigated excitatory synaptic transmission and plasticity using brain slices of MPTP treated animals. While L-LTP was blocked or significantly reduced. E-LTP was not significantly affected in slices of MPTP treated animals. LTD induced by repetitive stimulation was not affected. Furthermore, we found that paired-pulse facilitation and spontaneous release of glutamate were also altered in MPTP treated animals, suggesting presynaptic enhancement of excitatory transmission in PD. Our results suggest that ACC synaptic transmission is enhanced in the animal model of PD, and cortical excitation may play important roles in PD related pain and anxiety. |
format |
article |
author |
Zhaoxiang Zhou Penghai Ye Xu-Hui Li Yuxiang Zhang Muhang Li Qi-Yu Chen Jing-Shan Lu Man Xue Yanan Li Weiqi Liu Lin Lu Wantong Shi Ping-Yi Xu Min Zhuo |
author_facet |
Zhaoxiang Zhou Penghai Ye Xu-Hui Li Yuxiang Zhang Muhang Li Qi-Yu Chen Jing-Shan Lu Man Xue Yanan Li Weiqi Liu Lin Lu Wantong Shi Ping-Yi Xu Min Zhuo |
author_sort |
Zhaoxiang Zhou |
title |
Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease |
title_short |
Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease |
title_full |
Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease |
title_fullStr |
Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease |
title_full_unstemmed |
Synaptic potentiation of anterior cingulate cortex contributes to chronic pain of Parkinson’s disease |
title_sort |
synaptic potentiation of anterior cingulate cortex contributes to chronic pain of parkinson’s disease |
publisher |
BMC |
publishDate |
2021 |
url |
https://doaj.org/article/8d3f98e132d14b2b9478cacc6a82f1e6 |
work_keys_str_mv |
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