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The effection of neural apoptosis in the hippocampal formation of rats modal with congenital EDNRB gene defect

Authors :
XIE Dan
SONG Zan⁃min
WANG Xia
ZHANG Yong⁃bo
Source :
Chinese Journal of Contemporary Neurology and Neurosurgery, Vol 21, Iss 10, Pp 881-886 (2021)
Publication Year :
2021
Publisher :
Tianjin Huanhu Hospital, 2021.

Abstract

Objective The purpose of this study is to investigate apoptosis of hippocampal neurons and the expression of glial cell line⁃derived neurotrophic factor (GDNF) and brain⁃derived neurotrophic factor (BDNF) in neonatal pups with EDNRB gene deficiency. Methods The infant rats (2-3 d after birth) with EDNRB gene defect caused by congenital base deletion were divided into wild (+/+), heterozygous (+/sl) and homozygous (sl/sl), 6-8 rats were included in each group. Apoptosis of hippocampal nerve cells was detected by TUNEL staining. The number of apoptotosic cells was calculated by confocal fluorescence microscopy, and the levels of GDNF and BDNF in hippocampus was determined by enzyme⁃linked immunsorbent assay (ELISA). Results The number of apoptotic cells in hippocampus of the three genotypes was significantly different (F=24.315, P=0.000), the number of apoptotic cells in sl/sl was higher than that in +/+ (t=⁃6.780, P=0.000) and +/sl (t=4.801, P=0.000). The number of apoptotic cells was the highest in hippocampal CA1 region, followed by CA3 region, and the lowest in dentate gyrus. However, there was no significant difference in the levels of BDNF (F=0.766, P=0.479) and GDNF (F=2.538, P=0.107) in the hippocampus between different genotypes. Conclusions In rat with EDNRB gene defect, compared with the heterozygote and wild rats, the neural apoptosis were increased in hippocampal CA1, CA3 regions. But the levels of neurotrophic factors BDNF and GDNF were not significantly changed.

Details

Language :
English, Chinese
ISSN :
16726731
Volume :
21
Issue :
10
Database :
Directory of Open Access Journals
Journal :
Chinese Journal of Contemporary Neurology and Neurosurgery
Publication Type :
Academic Journal
Accession number :
edsdoj.75f52c541d034b96a4e46a77445eb31e
Document Type :
article
Full Text :
https://doi.org/10.3969/j.issn.1672⁃6731.2021.10.009