TY - JOUR
T1 - Prenatal stress in rat causes long-term spatial memory deficit and hippocampus MRI abnormality
T2 - Differential effects of postweaning enriched environment
AU - Lui, Chun Chung
AU - Wang, Jia Yi
AU - Tain, You Lin
AU - Chen, Yu Chieh
AU - Chang, Kow Aung
AU - Lai, Ming Chi
AU - Huang, Li Tung
N1 - Funding Information:
This study was supported by a grant from the National Science Council, Taiwan ( NSC-99-2314-B-182A-003 ) to Li-Tung Huang, and 99-2320-B-038-006-MY3 to Jia-Yi Wang.
Copyright:
Copyright 2012 Elsevier B.V., All rights reserved.
PY - 2011/2
Y1 - 2011/2
N2 - Prenatal stress (PS) can cause long-term hippocampus alternations in structure and plasticity in adult offspring. Enriched environment (EE) has an effect in rescuing a variety of neurological disorders. Pregnant dams were left undisturbed (prenatal control, PC) or restrained 6 h per day from days 14 to 21 (prenatal stress, PS). Control and prenatal stressed offspring rats were subjected to a standard rearing environment (SE) or an EE on postnatal days 22-120 (PC/SE PC/EE, PS/SE, and PS/EE; n = 5, each group). At ∼4 months of age, all rats underwent Morris water maze test and brain MRI examination. Hippocampi were then dissected for biochemical analyses, including, Western blot for NMDA receptor (NR) subunits and synaptophysin and RT-PCR forβ1 integrin and tissue-plasminogen activator (t-PA). MRI showed all 5 rats in the PS/SE group and 5 in the PS/EE group exhibited increased signals in bilateral hippocampus and increased T2 time in the PS/SE group. Exposure to EE treatment on postnatal days 22-120 counteracted the deficit in spatial memory and increased NR1 protein expression, but it did not affect the rate of high signals and increased T2 time, decreased NR2, synaptophysin, β1 integrin and t-PA mRNA expressions in PS adult offspring. The results of this study indicate PS in rats causes long-term spatial memory deficits and gross hippocampus pathology. Postnatal EE treatment has differential benefits in terms of spatial learning, signaling molecules, and gross hippocampus pathology.
AB - Prenatal stress (PS) can cause long-term hippocampus alternations in structure and plasticity in adult offspring. Enriched environment (EE) has an effect in rescuing a variety of neurological disorders. Pregnant dams were left undisturbed (prenatal control, PC) or restrained 6 h per day from days 14 to 21 (prenatal stress, PS). Control and prenatal stressed offspring rats were subjected to a standard rearing environment (SE) or an EE on postnatal days 22-120 (PC/SE PC/EE, PS/SE, and PS/EE; n = 5, each group). At ∼4 months of age, all rats underwent Morris water maze test and brain MRI examination. Hippocampi were then dissected for biochemical analyses, including, Western blot for NMDA receptor (NR) subunits and synaptophysin and RT-PCR forβ1 integrin and tissue-plasminogen activator (t-PA). MRI showed all 5 rats in the PS/SE group and 5 in the PS/EE group exhibited increased signals in bilateral hippocampus and increased T2 time in the PS/SE group. Exposure to EE treatment on postnatal days 22-120 counteracted the deficit in spatial memory and increased NR1 protein expression, but it did not affect the rate of high signals and increased T2 time, decreased NR2, synaptophysin, β1 integrin and t-PA mRNA expressions in PS adult offspring. The results of this study indicate PS in rats causes long-term spatial memory deficits and gross hippocampus pathology. Postnatal EE treatment has differential benefits in terms of spatial learning, signaling molecules, and gross hippocampus pathology.
KW - Enriched environment
KW - Magnetic resonance image
KW - NMDA receptors
KW - Prenatal stress
KW - Spatial learning
KW - T2 relaxation time
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U2 - 10.1016/j.neuint.2011.01.002
DO - 10.1016/j.neuint.2011.01.002
M3 - Article
C2 - 21215782
AN - SCOPUS:79951581070
SN - 0197-0186
VL - 58
SP - 434
EP - 441
JO - Neurochemistry International
JF - Neurochemistry International
IS - 3
ER -