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Neuropathic Itch
 
 
Article

Deletion of Acid-Sensing Ion Channel 3 Relieves the Late Phase of Neuropathic Pain by Preventing Neuron Degeneration and Promoting Neuron Repair

1
Department of Life Sciences, National Central University, Zhongli, Taoyuan City 32001, Taiwan
2
Division of Anesthesiology, Fu Jen Catholic University Hospital, New Taipei City 242062, Taiwan
3
School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei City 242062, Taiwan
4
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK
5
Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 11221, Taiwan
*
Author to whom correspondence should be addressed.
Cells 2020, 9(11), 2355; https://doi.org/10.3390/cells9112355
Received: 8 July 2020 / Revised: 16 October 2020 / Accepted: 22 October 2020 / Published: 26 October 2020
Neuropathic pain is one type of chronic pain that occurs as a result of a lesion or disease to the somatosensory nervous system. Chronic excessive inflammatory response after nerve injury may contribute to the maintenance of persistent pain. Although the role of inflammatory mediators and cytokines in mediating allodynia and hyperalgesia has been extensively studied, the detailed mechanisms of persistent pain or whether the interactions between neurons, glia and immune cells are essential for maintenance of the chronic state have not been completely elucidated. ASIC3, a voltage-insensitive, proton-gated cation channel, is the most essential pH sensor for pain perception. ASIC3 gene expression is increased in dorsal root ganglion neurons after inflammation and nerve injury and ASIC3 is involved in macrophage maturation. ASIC currents are increased after nerve injury. However, whether prolonged hyperalgesia induced by the nerve injury requires ASIC3 and whether ASIC3 regulates neurons, immune cells or glial cells to modulate neuropathic pain remains unknown. We established a model of chronic constriction injury of the sciatic nerve (CCI) in mice. CCI mice showed long-lasting mechanical allodynia and thermal hyperalgesia. CCI also caused long-term inflammation at the sciatic nerve and primary sensory neuron degeneration as well as increased satellite glial expression and ATF3 expression. ASIC3 deficiency shortened mechanical allodynia and attenuated thermal hyperalgesia. ASIC3 gene deletion shifted ATF3 expression from large to small neurons and altered the M1/M2 macrophage ratio, thereby preventing small neuron degeneration and relieved pain. View Full-Text
Keywords: neuropathic pain; acid-sensing ion channel 3; activating transcription factor 3; M1; M2 macrophages; nociceptors neuropathic pain; acid-sensing ion channel 3; activating transcription factor 3; M1; M2 macrophages; nociceptors
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MDPI and ACS Style

Kung, C.-C.; Huang, Y.-C.; Hung, T.-Y.; Teng, C.-Y.; Lee, T.-Y.; Sun, W.-H. Deletion of Acid-Sensing Ion Channel 3 Relieves the Late Phase of Neuropathic Pain by Preventing Neuron Degeneration and Promoting Neuron Repair. Cells 2020, 9, 2355. https://doi.org/10.3390/cells9112355

AMA Style

Kung C-C, Huang Y-C, Hung T-Y, Teng C-Y, Lee T-Y, Sun W-H. Deletion of Acid-Sensing Ion Channel 3 Relieves the Late Phase of Neuropathic Pain by Preventing Neuron Degeneration and Promoting Neuron Repair. Cells. 2020; 9(11):2355. https://doi.org/10.3390/cells9112355

Chicago/Turabian Style

Kung, Chia-Chi, Yi-Chu Huang, Ting-Yun Hung, Chih-Yu Teng, Tai-Ying Lee, and Wei-Hsin Sun. 2020. "Deletion of Acid-Sensing Ion Channel 3 Relieves the Late Phase of Neuropathic Pain by Preventing Neuron Degeneration and Promoting Neuron Repair" Cells 9, no. 11: 2355. https://doi.org/10.3390/cells9112355

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