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Neonatal ketamine exposure-induced hippocampal neuroapoptosis in the developing brain impairs adult spatial learning ability

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Neural Regeneration Research 2020年第5期15卷 880-886页

作者： Dan Lyu Ning Tang Andrew W. Womack Yong-Jin He Qing Lin Department of Pain Management Tianjin First Center HospitalTianjinChina Department of Psychology College of ScienceUniversity of Texas at ArlingtonArlingtonTXUSA Reproductive Medicine Center the 960^th Hospital of the PLA Joint Logistics Support ForceJinanShandong ProvinceChina

Ketamine exposure can lead to selective neuroapoptosis in the developing brain.p66ShcA,the cellular adapter protein expressed selectively in immature neurons,is a known pro-apoptotic molecule that triggers neuroapoptosis when ***-Dawley rats at postnatal day 7 were subcutaneously injected in the neck with ketamine 20 mg/kg,six times at 2-hour *** 0,1,3,and 6 hours after final injection,western blot assay was used to detect the expression of cleaved caspase-3,p66ShcA,and phosphorylated *** found that the expression of activated p66ShcA and caspase-3 increased after ketamine exposure and peaked at 3 *** same procedure was performed on a different group of *** the age of 4 weeks,spatial learning and memory abilities were tested with the Morris water *** to find the hidden platform for these rats was longer than it was for control rats,although the residence time in the target quadrant was *** findings indicate that ketamine exposure resulted in p66ShcA being activated in the course of an apoptotic cascade during the neonatal *** may have contributed to the deficit in spatial learning and memory that persisted into *** experimental protocol was approved by the Institutional Animal Care and Use Committee at the University of Texas at Arlington,USA (approval No.A13.008) on January 22,2013.

关键词： caspase-3 developmental neuroapoptosis hippocampus ketamine Morris water maze N-methyl-D-aspartate acid receptors p66ShcA spatial learning

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Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2017年第9期18卷 789-796页

作者： Ning ZHANG Quan-ping SU Wei-xia ZHANG Nian-jun SHI Hao ZHANG Ling-ping WANG Zhong-kai LIU Ke-zhong LI Department of Anesthesiology the Second Hospital of Shandong University Department of Anesthesiology Linyi People’s Hospital The Central Laboratory Linyi Peoples’ Hospital Intensive Care Unit Linyi People’s Hospital

The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell viability was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. Then neurons were pretreated with different concentrations of dexmedetomidine before 100 μmol/L propofol was added. Akt, phospho-Akt(p-Akt), Bad, phospho-Bad(p-Bad), and Bcl-x L were detected by Western blot. Also, neurons were pretreated with dexmedetomidine alone or given the inhibitor LY294002 before dexmedetomidine pretreatment, and then propofol was added for 3h. The results demonstrated that propofol decreased the cell viability and the expression of p-Akt and p-Bad proteins, increased the level of Bad, and reduced the ratio of Bcl-x L/Bad. Dexmedetomidine pretreatment could reverse these effects. The enhancement of p-Akt and p-Bad induced by dexmedetomidine was prevented by LY294002. These results showed that dexmedetomidine potently protected the developing neuron and this protection may be partly mediated by the PI3K/Akt pathway.

关键词： Dexmedetomidine Propofol neuroapoptosis PI3K/Akt

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Expression of the apoptosis related proteins,caspase-3 and NF-κB,in the hippocampus of Tg2576 mice

Expression of the apoptosis related proteins,caspase-3 and N...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Yan-Li NIU,Wei-Juan ZHANG,Bin LIU,Guo-Tao SUN,Dong-Ming YU,Ming-Shan LI,Jin-Bo DENG~* Institute of Neurobiology and Laboratory of Neurobiology,Medical College of Henan University,Kaifeng 475004, China

＜正＞The goal of the current study was to gain a better understanding of the relationship between neuroapoptosis and development of Alzheimer’s disease,with an emphasis on the role of NF-κB in *** CA3 region of the hippocampus in Tg2576（APPswe） transgenic mice was studied from postnatal day 0 to postnatal day 180 using a combination of HE staining,Niss1 method and immunohistochemistry to detect caspase-3 and NF-κB（p50） *** results demonstrated that overall neuroapoptosis and NF-κB activity decreased gradually with increasing age in both wild type and Tg2576 ***,the number of caspase-3 positive or NF-κB positive pyramidal cells in Tg2576 mice was greater than that in wild type mice of the same age,with significant differences after P14（P＜0.01 or P＜0.05）.Linear regression analysis of caspase-3 and NF-κB expression demonstrated a correlation between neuroapoptosis and activity of NF-κ*** together,our results suggest that the process of neuroapoptosis is consistent with the onset and development of Alzheimer’s ***,the observed correlation between neuroapoptosis and NF-κB activity suggests a role for NF-κB in hippocampal neuroapoptosis.

关键词： Alzheimer’s disease APPswe transgenic mice caspase-3 hippocampus neuroapoptosis NF-κB

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