4.7 Article

PRG-1 prevents neonatal stimuli-induced persistent hyperalgesia and memory dysfunction via NSF/Glu/GluR2 signaling

期刊

ISCIENCE
卷 25, 期 9, 页码 -

出版社

CELL PRESS
DOI: 10.1016/j.isci.2022.104989

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资金

  1. National Natural Science Foundation of China [81960217, 81760214]
  2. Major research project of innovation group in Education Department of Guizhou Province [QianJiaoHe KY [2017] 043]
  3. Doctoral Scientific Research Startup Fund Project of Zunyi Medical University [F-954]
  4. Guizhou Provincial Science and Technology Planning Project [QianKeHe JiChu ZK [2021] 410]

向作者/读者索取更多资源

Repetitive noxious stimuli in neonates have long-term harmful effects on nociceptive processing, learning, and memory. Plasticity-related gene 1 (PRG-1) regulates synaptic plasticity and functional reorganization in the brain. This study shows that neonatal repetitive noxious stimuli lead to hyperalgesia, allodynia, and impairments in learning and memory, which are associated with the interaction between PRG-1 and N-ethylmaleimide sensitive fusion protein (NSF), enhanced glutamate release, and deficiency in AMPAR GluR2 trafficking.
Neonatal repetitive noxious stimuli (RNS) has been shown to cause long-term harmful effects on nociceptive processing, learning, and memory which persist until adulthood. Plasticity-related gene 1 (PRG-1) regulates synaptic plasticity and functional reorganization in the brain during neuronal development. In this study, neonatal RNS rats were established by repetitive needle pricks to neonatal rats on all four feet to model repetitive pain exposure in infants. Neonatal RNS caused thermal hyperalgesia, mechanical allodynia, learning, and memory impairments which manifested in young rats and persisted until adulthood. Hippocampal PRG-1/N-ethylmaleimide sensitive fusion protein (NSF) interaction was determined to be responsible for the RNS-induced impairment via enhanced extracellular glutamate release and AMPAR GluR2 trafficking deficiency in a cell-autonomous manner. These pathways likely act synergistically to cause changes in dendritic spine density. Our findings suggest that PRG-1 prevents the RNS-induced hyperalgesia, learning, and memory impairment by regulating synaptic plasticity via NSF/Glu/GluR2 signaling.

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