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Cranial irradiation impairs intrinsic excitability and synaptic plasticity of hippocampal CA1 pyramidal neurons with implications for cognitive function

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Neural Regeneration Research 2022年第10期17卷 2253-2259页

作者： Min-Yi Wu Wen-Jun Zou Pei Yu Yuhua Yang Shao-Jian Li Qiang Liu Jiatian Xie Si-Qi Chen Wei-Jye Lin Yamei Tang Department of Neurology Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina State Key Laboratory of Organ Failure Research Key Laboratory of Mental Health of the Ministry of EducationGuangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired IntelligenceKey Laboratory of Psychiatric Disorders of Guangdong ProvinceCollaborative Innovation Center for Brain ScienceDepartment of NeurobiologySouthern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Anesthesiology Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Guangdong-Hong Kong Joint Laboratory for RNA MedicineSun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Medical Research Center Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Guangdong Province Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina

Radiation therapy is a standard treatment for head and neck tumors.However,patients often exhibit cognitive impairments following radiation therapy.Previous studies have revealed that hippocampal dysfunction,specifically abnormal hippocampal neurogenesis or neuroinflammation,plays a key role in radiation-induced cognitive impairment.However,the long-term effects of radiation with respect to the electrophysiological adaptation of hippocampal neurons remain poorly characterized.We found that mice exhibited cognitive impairment 3 months after undergoing 10 minutes of cranial irradiation at a dose rate of 3 Gy/min.Furthermore,we observed a remarkable reduction in spike firing and excitatory synaptic input,as well as greatly enhanced inhibitory inputs,in hippocampal CA1 pyramidal neurons.Corresponding to the electrophysiological adaptation,we found reduced expression of synaptic plasticity marker VGLUT1 and increased expression of VGAT.Furthermore,in irradiated mice,long-term potentiation in the hippocampus was weakened and glur1 expression was inhibited.These findings suggest that radiation can impair intrinsic excitability and synaptic plasticity in hippocampal CA1 pyramidal neurons.

关键词： GABA-mediated hyperfunction glur intrinsic excitability long-term potentiation radiation-induced cognitive impairment spontaneous excitatory postsynaptic currents spontaneous inhibitory postsynaptic currents synaptic plasticity type I vesicular glutamate transporter vesicular GABA transporter whole-cell patch clamp recording

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Neuroprotective effects of autophagy inhibition on hippocampal glutamate receptor subunits after hypoxia-ischemia-induced brain damage in newborn rats

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Neural Regeneration Research 2017年第3期12卷 417-424页

作者： Li-xiao Xu Xiao-juan Tang Yuan-yuan Yang Mei Li Mei-fang Jin Po Miao Xin Ding Ying Wang Yan-hong Li Bin Sun Xing Feng Institute of Pediatric Research Affiliated Children's Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Department of Neonatology Affiliated Children's Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina

Autophagy has been suggested to participate in the pathology of hypoxic-ischemic brain damage（HIBD）.However,its regulatory role in HIBD remains unclear and was thus examined here using a rat model.To induce HIBD,the left common carotid artery was ligated in neonatal rats,and the rats were subjected to hypoxia for 2 hours.Some of these rats were intraperitoneally pretreated with the autophagy inhibitor 3-methyladenine（10 m M in 10 μL） or the autophagy stimulator rapamycin（1 g/kg） 1 hour before artery ligation.Our findings demonstrated that hypoxia-ischemia-induced hippocampal injury in neonatal rats was accompanied by increased expression levels of the autophagy-related proteins light chain 3 and Beclin-1 as well as of the AMPA receptor subunit glur 1,but by reduced expression of glur 2.Pretreatment with the autophagy inhibitor 3-methyladenine blocked hypoxia-ischemia-induced hippocampal injury,whereas pretreatment with the autophagy stimulator rapamycin significantly augmented hippocampal injury.Additionally,3-methyladenine pretreatment blocked the hypoxia-ischemia-induced upregulation of Glu R1 and downregulation of glur2 in the hippocampus.By contrast,rapamycin further elevated hippocampal Glu R1 levels and exacerbated decreased glur2 expression levels in neonates with HIBD.Our results indicate that autophagy inhibition favors the prevention of HIBD in neonatal rats,at least in part,through normalizing Glu R1 and glur2 expression.

关键词： nerve regeneration hypoxic-ischemic brain damage hypoxia ischemia α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptor subunit glur hippocampus rapamycin 3-methyladenine neural regeneration

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