title: Effects of Chronic Stress on Cognition in Male SAMP8 Mice.
abstract: OBJECTIVE
  Chronic stress can lead to cognitive impairment. Senescence-accelerated mouse prone 8 (SAMP8) is a naturally occurring animal model that is useful for investigating the neurological mechanisms of Alzheimer's disease. Here we investigated the impact and mechanisms of chronic stress on cognition in male SAMP8 mice.
  
  
  METHODS
  Male 6-month- old SAMP8 and SAMR1 (senescence-accelerated mouse resistant 1) mice strains were randomly divided into 4 groups. Mice in the unpredictable chronic mild stress (UCMS) groups were exposed to diverse stressors for 4 weeks. Then, these mice performed Morris water maze (MWM) test to assess the effect of UCMS on learning and memory. To explore the neurological mechanisms of UCMS on cognition in mice, we evaluated changes in the expression of postsynaptic density 95 (PSD95) and synaptophysin (SYN), which are essential proteins for synaptic plasticity. Five mice from each group were randomly chosen for reverse transcription polymerase chain reaction (RT-PCR) and western blotting analysis of SYN and PSD95.
  
  
  RESULTS
  The Morris water maze experiment revealed that the cognitive ability of the SAMP8 mice decreased with brain aging, and that chronic stress aggravated this cognitive deficit. In addition, chronic stress decreased the mRNA and protein expression of SYN and PSD95 in the hippocampus of the SAMP8 mice; however, the SAMR1 mice were unaffected.
  
  
  CONCLUSIONS
  Our results demonstrate that decreased cognition and synaptic plasticity are related to aging. Moreover, we show that chronic stress aggravated this cognitive deficit and decreased SYN and PSD95 expression in the SAMP8 mice. Furthermore, the SAMP8 mice were more vulnerable to the detrimental effects of chronic stress on cognition than the SAMR1 mice. Our results suggest that the neurological mechanisms of chronic stress on cognition might be associated with a decrease in hippocampal SYN and PSD95 expression, which is critical for structural synaptic plasticity.
authors: Department of Neurology, the First Hospital of Hebei Medical University, Shijiazhuang, PR China.
authors: Jinhua
authors: J
authors: Wang
authors: Jie
authors: J
authors: Yuan
authors: Jingjuan
authors: J
authors: Pang
authors: Jiang
authors: J
authors: Ma
authors: Bing
authors: B
authors: Han
authors: Yuan
authors: Y
authors: Geng
authors: Li
authors: L
authors: Shen
authors: Hualong
authors: H
authors: Wang
authors: Qinying
authors: Q
authors: Ma
authors: Yanyong
authors: Y
authors: Wang
authors: Mingwei
authors: M
authors: Wang
mesh_terms: D000375:Aging / Q000235:genetics* / Q000473:pathology; D000544:Alzheimer Disease / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D003071:Cognition; D004195:Disease Models, Animal; D000076122:Disks Large Homolog 4 Protein; D005786:Gene Expression Regulation; D051528:Guanylate Kinases / Q000235:genetics* / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D018782:Maze Learning; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism; D008568:Memory; D051379:Mice; D009473:Neuronal Plasticity; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013045:Species Specificity; D013315:Stress, Psychological / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D016708:Synaptophysin / Q000235:genetics* / Q000378:metabolism
chemical_list: D000076122:Disks Large Homolog 4 Protein; C501447:Dlg4 protein, mouse; D008565:Membrane Proteins; D012333:RNA, Messenger; D016708:Synaptophysin; C569015:Syp protein, mouse; D051528:Guanylate Kinases