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Attractin Gene Deficiency in Rats Leads to Impairments in Both Activity and Spatial Learning and Memory.

Authors
  • Li, Xiao-Hui1
  • Xue, Cheng2
  • Liu, Meng-Qi1
  • Zhang, Meng-Yu1
  • Zhou, Yang1
  • Xiao, Xu1
  • Wang, Jia1
  • Xu, Xi-Jia3
  • Shi, Yun4
  • Zhang, Wei-Ning5
  • 1 School of Medicine, Jiangsu University, Zhenjiang 212013, Jiangsu Province, PR China. , (China)
  • 2 School of Medicine, Jiangsu University, Zhenjiang 212013, Jiangsu Province, PR China; Department of Clinical Laboratory, Affiliated Changzhou No.2 People's Hospital, Nanjing Medical University, Changzhou 213003, PR China. , (China)
  • 3 Department of Psychiatry, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, PR China. Electronic address: [email protected] , (China)
  • 4 Ministry of Education Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210032, PR China. Electronic address: [email protected] , (China)
  • 5 School of Medicine, Jiangsu University, Zhenjiang 212013, Jiangsu Province, PR China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Neuroscience
Publication Date
May 14, 2021
Identifiers
DOI: 10.1016/j.neuroscience.2021.05.006
PMID: 34000322
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Attractin (ATRN), an autosomal recessive gene that is widely distributed in the brain, is involved in the execution of a variety of brain functions and associated with certain neuropsychiatric disorders. Here, we introduce a novel rat strain harboring a mutation in ATRN that was generated by knocking in ATRN-G505C via the CRISPR/Cas9 system. We assessed the behavioral performance of these mutant ATRN knock-in rats. The G505C mutation was introduced into exon 9, and a synthetic primer was inserted into introns 8-9 for genotyping. The 505th amino acid, a Gly (G) residue, was mutated to a Cys (C) residue, i.e., GGC was mutated to TGC. Behavioral experiments showed that homozygous ATRN rats spent significantly more time searching for the escape platform in the acquisition trial and significantly less time in the target area in the probe trial in the Morris water maze (MWM) test and traveled a significantly shorter distance in the open field test (OFT) than wild-type rats. In addition, Western blot analysis and immunohistochemistry showed that rats with the mutant ATRN gene exhibited significantly reduced expression of brain-derived neurotrophic factor (BDNF). In summary, our results indicate that mutations in the ATRN gene directly lead to learning and memory impairments and slight motor deficits. These findings provide new clues for the mechanism by which mutant ATRN induces neurodegenerative changes. Copyright © 2021 IBRO. Published by Elsevier Ltd. All rights reserved.

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