Prenatal stress in rat causes long-term spatial memory deficit and hippocampus MRI abnormality: Differential effects of postweaning enriched environment

• Published in: Neurochemistry international Vol. 58; no. 3; pp. 434 - 441
• Main Authors: Lui, Chun Chung, Wang, Jia-Yi, Tain, You-Lin, Chen, Yu-Chieh, Chang, Kow-Aung, Lai, Ming-Chi, Huang, Li-Tung
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.02.2011; Elsevier
• Subjects: Animals; Biological and medical sciences; Disease Models, Animal; Enriched environment; Environment, Controlled; Female; Fundamental and applied biological sciences. Psychology; Hippocampus - pathology; Magnetic resonance image; Male; Memory Disorders - diagnosis; Memory Disorders - pathology; Memory Disorders - therapy; NMDA receptors; Pregnancy; Prenatal Exposure Delayed Effects - diagnosis; Prenatal Exposure Delayed Effects - pathology; Prenatal Exposure Delayed Effects - therapy; Prenatal stress; Rats; Rats, Sprague-Dawley; Spatial learning; Stress, Psychological - diagnosis; Stress, Psychological - pathology; Stress, Psychological - therapy; T2 relaxation time; Vertebrates: nervous system and sense organs; Weaning; EE; PS; NR; MRI; NMDA receptors; Spatial learning; SE; PC; T2 relaxation time; Magnetic resonance image; t-PA; Prenatal stress; Enriched environment; Memory disorder; Cognitive disorder; Rat; Central nervous system; Glutamate receptor; Space perception; Stimulating environment; Encephalon; Prenatal; Rodentia; Nuclear magnetic resonance imaging; Long term; Stress; Vertebrata; Mammalia; Animal; Perceptive learning; NMDA receptor; Hippocampus; Spatial memory
• ISSN: 0197-0186; 1872-9754
• DOI: 10.1016/j.neuint.2011.01.002

▶ Prenatal stress. ▶ Spatial deficit. ▶ Hippocampus MRI abnormality. ▶ Enriched environment. ▶ Differential therapeutic effects. 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 6h 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.