PRG-1 prevents neonatal stimuli-induced persistent hyperalgesia and memory dysfunction via NSF/Glu/GluR2 signaling.
PRG-1 prevents neonatal stimuli-induced persistent hyperalgesia and memory dysfunction via NSF/Glu/GluR2 signaling.
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DOI：
10.1016/j.isci.2022.104989
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发表时间：
2022-09-16
期刊：
影响因子：
5.8
通讯作者：
Xiao, Zhi
中科院分区：
文献类型：
--
作者：
Liu, Xingfeng;Li, Site;Zhang, Wenyu;Xie, Zhuo;He, Jingxin;Zhang, Xuanwei;Yu, Shouyang;Cao, Song;Yu, Tian;Xiao, Zhi
新生儿重复性伤害性刺激（RNS）已被证明会对伤害性处理、学习和记忆造成长期的有害影响，并持续到成年。可塑性相关基因1（PRG-1）在神经元发育过程中调节脑中突触可塑性和功能重组。在这项研究中，新生RNS大鼠建立了重复针刺新生大鼠的所有四只脚模型重复疼痛暴露的婴儿。新生RNS引起热痛觉过敏，机械异常性疼痛，学习和记忆障碍，表现在年轻大鼠，并持续到成年。海马PRG-1/N-乙基马来酰亚胺敏感性融合蛋白（NSF）的相互作用被确定为负责通过增强细胞外谷氨酸释放和AMPAR GluR 2运输缺陷的细胞自主的方式RNS-induced损害。这些途径可能协同作用，导致树突棘密度的变化。我们的研究结果表明，PRG-1通过NSF/Glu/GluR 2信号调节突触可塑性来防止RNS诱导的痛觉过敏，学习和记忆障碍。新生儿RNS诱导痛觉过敏，学习和记忆障碍，直到成年。PRG-1通过树突棘调节减弱RNS诱导的损伤。PRG-1通过NSF/Glu/GluR 2信号传导防止RNS诱导的损伤。行为神经科学;分子神经科学;发育神经科学;细胞神经科学
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. Neonatal RNS induced hyperalgesia, learning, and memory impairment until adulthood. PRG-1 attenuated RNS-induced impairments by dendritic spine regulation. PRG-1 prevents RNS-induced impairments via NSF/Glu/GluR2 signaling. Behavioral neuroscience; Molecular neuroscience; Developmental neuroscience; Cellular neuroscience
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