期刊
CELL REPORTS
卷 33, 期 6, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2020.108369
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资金
- National Natural Science Foundation of China [81961128024, 81571068, 31871062, 81801102, 31771157]
- Fundamental Research Funds for the Central Universities
- National Postdoctoral Science Foundation of China [2018M642413, 2019T120507]
- Key Realm R&D Program of Guangdong Province of China [2019B030335001]
Nerve injury in somatosensory pathways may lead to neuropathic pain, which affects the life quality of similar to 8% of people. Long-term enhancement of excitatory synaptic transmission along somatosensory pathways contributes to neuropathic pain. Caspase 3 (Casp3) plays a non-apoptotic role in the hippocampus and regulates internalization of, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits. Whether Casp3-AMPAR interaction is involved in the maintenance of peripheral hypersensitivity after nerve injury remained unknown. Here, we show that nerve injury suppresses long-term depression (LTD) and downregulates Casp3 in the anterior cingulate cortex (ACC). Interfering with interactions between Casp3 and AM-PAR subunits or reducing Casp3 activity in the ACC suppresses LTD induction and causes peripheral hypersensitivity. Overexpression of Casp3 restores LTD and reduces peripheral hypersensitivity after nerve injury. We reveal how Casp3 is involved in the maintenance of peripheral hypersensitivity. Our findings suggest that restoration of LTD via Casp3 provides a therapeutic strategy for neuropathic pain management.
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