PMID- 28855140
OWN - NLM
STAT- MEDLINE
DCOM- 20180601
LR  - 20181202
IS  - 1872-7549 (Electronic)
IS  - 0166-4328 (Linking)
VI  - 336
DP  - 2018 Jan 15
TI  - Prenatal stress induced gender-specific alterations of N-methyl-d-aspartate 
      receptor subunit expression and response to Abeta in offspring hippocampal cells.
PG  - 182-190
LID - S0166-4328(17)30670-8 [pii]
LID - 10.1016/j.bbr.2017.08.036 [doi]
AB  - Prenatal stress (PS) is one of adverse life events during pregnancy, which may 
      increase vulnerability to cognitive impairment in adult offspring. Abeta 
      synaptotoxicity is one important pathological factor for cognitive impairment, 
      and PS-induced cognitive disorder is closely associated with N-Methyl-d-Aspartate 
      receptor (NMDAR), which acts as a key mediator of Abeta synaptotoxicity. In the 
      present study, we tried to explore whether PS affects offspring's Abeta levels and 
      NMDAR subunit expression in a gender-specific manner in hippocampal CA and DG 
      subregions, and whether PS affects synaptic proteins and NMDAR subunit expression 
      in cultured offspring hippocampal cells exposed to Abeta. Pregnant SD rats with 
      restraint stress from gestation day 8-20 were used as PS model. Morris water 
      maze, ELISA, immunofluorescence and western blot were tested on postnatal day 90 
      in male and female PS offspring. Our results showed that female offspring is more 
      vulnerable to PS-induced cognitive impairment. Surprisingly, PS enhanced Abeta(1-40) 
      levels in the hippocampal DG subregion of male offspring. Furthermore, WB results 
      implied that the decreased GluN2A in CA of female may contribute to the 
      PS-induced cognitive impairment, while in DG, the increased GluN2A and decreased 
      GluN2B contributed to protective effects against Abeta. Interestingly, we found PS 
      could alleviate Abeta synaptotoxicity in male offspring's hippocampal cells. 
      Overall, our results provided a fundamental understanding of PS-induced 
      gender-specific alterations of NMDAR subunit expression and the susceptibility to 
      Abeta, and paved the road for the development of timely preventive interventions on 
      cognitive disorders of PS offspring.
CI  - Copyright (c) 2017. Published by Elsevier B.V.
FAU - Fang, Yuan
AU  - Fang Y
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Li, Hui
AU  - Li H
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Chang, Lirong
AU  - Chang L
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Song, Yizhi
AU  - Song Y
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Ma, Longhui
AU  - Ma L
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Lu, Liying
AU  - Lu L
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Du, Zunshu
AU  - Du Z
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Li, Yan
AU  - Li Y
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China.
FAU - Liu, Jinping
AU  - Liu J
AD  - School of Medicine, Tsinghua University, Beijing, China.
FAU - Wu, Yan
AU  - Wu Y
AD  - Department of Anatomy, Beijing Institute for Brain Disorders, Capital Medical 
      University, Beijing, China. Electronic address: yanwu@ccmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20170909
PL  - Netherlands
TA  - Behav Brain Res
JT  - Behavioural brain research
JID - 8004872
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (NR2B NMDA receptor)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - VH92ICR8HX (N-methyl D-aspartate receptor subtype 2A)
SB  - IM
MH  - Amyloid beta-Peptides/metabolism
MH  - Animals
MH  - Cognition Disorders/metabolism
MH  - Cognitive Dysfunction/metabolism
MH  - Female
MH  - Gene Expression Regulation/physiology
MH  - Hippocampus/*metabolism/physiopathology
MH  - Male
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/metabolism/*physiology
MH  - Sex Factors
MH  - Stress, Psychological/metabolism/*physiopathology
MH  - Temporal Lobe/metabolism
OTO - NOTNLM
OT  - Amyloid-beta
OT  - Cognitive impairment
OT  - Hippocampus
OT  - NMDAR subunit
OT  - Prenatal stress
EDAT- 2017/09/01 06:00
MHDA- 2018/06/02 06:00
CRDT- 2017/09/01 06:00
PHST- 2017/04/20 00:00 [received]
PHST- 2017/08/20 00:00 [revised]
PHST- 2017/08/23 00:00 [accepted]
PHST- 2017/09/01 06:00 [pubmed]
PHST- 2018/06/02 06:00 [medline]
PHST- 2017/09/01 06:00 [entrez]
AID - S0166-4328(17)30670-8 [pii]
AID - 10.1016/j.bbr.2017.08.036 [doi]
PST - ppublish
SO  - Behav Brain Res. 2018 Jan 15;336:182-190. doi: 10.1016/j.bbr.2017.08.036. Epub 
      2017 Sep 9.