CNS neuroscience & therapeutics · 2025
PRG-1 Relieves Neonatal Stimuli-Induced Hyperalgesia and Anxiety via Stage-Specific Synapse Remodeling.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhang Wenyu, Li Yan, Liang Guangda, Li Qingmei, Song Zhouyi, Cao Song, Xiao Zhi, Liu Xingfeng
Аннотация
OBJECTIVE: Neonatal repetitive noxious stimuli (RNS), to mimic early-life repetitive pain exposure, induce persistent hyperalgesia, anxiety-like behaviors and postoperative pain sensitization that endure into adulthood. These long-term neurobehavioral abnormalities are associated with impaired cognitive, emotional, and psychosocial functions.
METHOD: We established a neonatal RNS rat model through repetitive needle pricks to all four limbs of neonatal rats and investigated the effects of hippocampal PRG-1 and synaptic remodeling at different stages in RNS rat.
RESULTS: Our study demonstrates that hippocampal PRG-1 dynamically modulates RNS-induced hyperalgesia and anxiety through stage-specific regulation of AMPAR GluR1/GluR2 and NMDAR GluN2A/GluN2B trafficking, which leads to synaptic remodeling via altered dendritic synaptic morphology and synaptic transmission efficacy.
CONCLUSION: Our findings suggest that PRG-1 relieves RNS-induced persistent hyperalgesia, anxiety, and pain-perception memory via synapse remodeling at different stages. Targeting PRG-1-mediated synaptic remodeling may provide a novel neuroprotective strategy for preventing chronic pain comorbidities with anxiety disorders following early-life pain exposure.
METHOD: We established a neonatal RNS rat model through repetitive needle pricks to all four limbs of neonatal rats and investigated the effects of hippocampal PRG-1 and synaptic remodeling at different stages in RNS rat.
RESULTS: Our study demonstrates that hippocampal PRG-1 dynamically modulates RNS-induced hyperalgesia and anxiety through stage-specific regulation of AMPAR GluR1/GluR2 and NMDAR GluN2A/GluN2B trafficking, which leads to synaptic remodeling via altered dendritic synaptic morphology and synaptic transmission efficacy.
CONCLUSION: Our findings suggest that PRG-1 relieves RNS-induced persistent hyperalgesia, anxiety, and pain-perception memory via synapse remodeling at different stages. Targeting PRG-1-mediated synaptic remodeling may provide a novel neuroprotective strategy for preventing chronic pain comorbidities with anxiety disorders following early-life pain exposure.