Dynamic alteration of dendrites and dendritic spines in the hippocampus and microglia in mouse brain tissues after kainate-induced status epilepticus

Author(s):  
Lingling Xie ◽  
Tianyi Li ◽  
Xiaojie Song ◽  
Hong Sun ◽  
Jie Liu ◽  
...  
2020 ◽  
Vol 16 ◽  
Author(s):  
Dang Kim Thu ◽  
Dao Thi Vui ◽  
Nguyen Thi Ngoc Huyen ◽  
Nguyen Thi Thanh Binh ◽  
Nguyen Thi Huyen ◽  
...  

Background: Huperzia phlegmaria has been used for the treatment of neurological disorder. Alkaloids are main bioactive compounds found in Huperzia phlegmaria. We aimed to investigate the acetylcholinesterase (AChE) inhibitory activity in vitro of Huperzia phlegmaria alkaloid extract (HpAE) and protective effects on mice which were induced cognitive deficits by scopolamine. Methods: AChE inhibitory activity and kinetic inhibition mechanism was investigated by Ellman's assay. Mice were administrated orally HpAE (30 mg/kg and 60 mg/kg) for fourteen days, and injected scopolamine at a dose of 1 mg/kg intraperitoneally for four days to induce cognitive impairment. The Y-maze and the Morris water maze were used for evaluating the memory behaviors. Acetylcholine (ACh) levels and AChE activity were measured in brain tissue. Glutathione peroxidase (GPx), superoxide dismutase (SOD) activities, and malondialdehyde (MDA) groups were also evaluated in the mouse brain tissues. Results: Our data showed that HpAE had the strong AChE inhibitory activity with an IC50 value of 5.12 ± 0.48 μg/mL in a concentration-dependent manner. Kinetic inhibition analysis demonstrated that HpPAE inhibited AChE followed the mixed inhibition type with Ki (representing the affinity of the enzyme and inhibitor) was 4.37 ± 0.35 µg/mL. Scopolamine induced the cognitive impairment in Morris Water Maze and Y-maze test along with reduced brain levels of ACh and antioxidant enzyme and increased AChE activity in mouse brain tissues. Treatment with HpAE at both dose (30 mg/kg and 60 mg/kg) decreased the SCP-induced cognitive impairment in both behavioral tests along with decreased acetylcholinesterase activity and MDA level, and increased ACh level and antioxidant enzyme in mouse brain tissues. Conclusion: Our results suggested that the HpAE at both dose (30 mg/kg and 60 mg/kg) may be used for prevent and treatment of Alzheimer’s disease.


2016 ◽  
Vol 1642 ◽  
pp. 546-552 ◽  
Author(s):  
Zhigang Miao ◽  
Ning Xin ◽  
Bin Wei ◽  
Xiaodong Hua ◽  
Gaocai Zhang ◽  
...  
Keyword(s):  

Methods ◽  
2020 ◽  
Vol 177 ◽  
pp. 35-49 ◽  
Author(s):  
Satoshi Muraoka ◽  
Weiwei Lin ◽  
Mei Chen ◽  
Samuel W. Hersh ◽  
Andrew Emili ◽  
...  

2007 ◽  
Vol 1150 ◽  
pp. 225-238 ◽  
Author(s):  
Estíbaliz Ampuero ◽  
Alexies Dagnino-Subiabre ◽  
Rodrigo Sandoval ◽  
Rodrigo Zepeda-Carreño ◽  
Soledad Sandoval ◽  
...  

Glycobiology ◽  
2020 ◽  
Author(s):  
Yuhsuke Ohmi ◽  
Takashi Nishikaze ◽  
Yoko Kitaura ◽  
Takako Ito ◽  
Satoko Yamamoto ◽  
...  

Abstract Sialic acids are unique sugars with negative charge and exert various biological functions such as regulation of immune systems, maintenance of nerve tissues and expression of malignant properties of cancers. Alpha 2,6 sialylated N-glycans, one of representative sialylation forms, are synthesized by St6gal1 or St6gal2 gene products in humans and mice. Previously, it has been reported that St6gal1 gene is ubiquitously expressed in almost all tissues. On the other hand, St6gal2 gene is expressed mainly in the embryonic and perinatal stages of brain tissues. However, roles of St6gal2 gene have not been clarified. Expression profiles of N-glycans with terminal α2,6 sialic acid generated by St6gal gene products in the brain have never been directly studied. Using conventional lectin blotting and novel sialic acid linkage-specific alkylamidationmass spectrometry method (SALSA-MS), we investigated the function and expression of St6gal genes and profiles of their products in the adult mouse brain by establishing KO mice lacking St6gal1 gene, St6gal2 gene, or both of them (double knockout). Consequently, α2,6-sialylated N-glycans were scarcely detected in adult mouse brain tissues, and a majority of α2,6-sialylated glycans found in the mouse brain were O-linked glycans. The majority of these α2,6-sialylated O-glycans were shown to be disialyl-T antigen and sialyl-(6)T antigen by mass spectrometry analysis. Moreover, it was revealed that a few α2,6-sialylated N-glycans were produced by the action of St6gal1 gene, despite both St6gal1 and St6gal2 genes being expressed in the adult mouse brain. In the future, where and how sialylated O-linked glycoproteins function in the brain tissue remains to be clarified.


2014 ◽  
Vol 6 (2) ◽  
Author(s):  
Michael A. Meyer

As the CA1 sector has been implicated to play a key role in memory formation, a dedicated search for highly expressed genes within this region was made from an on-line atlas of gene expression within the mouse brain (GENSAT). From a data base of 1013 genes, 16 were identified that had selective localization of gene expression within the CA1 region, and included <em>Angpt2, ARHGEF6, CCK, Cntnap1, DRD3, EMP1, Epha2, Itm2b, Lrrtm2, Mdk, PNMT, Ppm1e, Ppp2r2d, RASGRP1, Slitrk5,</em> and <em>Sstr4</em>. Of the 16 identified, the most selective and intense localization for both adult and post-natal day 7 was noted for <em>ARHGEF6</em>, which is known to be linked to non-syndromic mental retardation, and has also been localized to dendritic spines. Further research on the role played by <em>ARHGEF6</em> in memory formation is strongly advocated.


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