Effects of isoflurane exposure during pregnancy on postnatal memory and learning in offspring rats |
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Authors: | Fei-juan Kong Yu-wen Tang Ai-fei Lou Hong Chen Lin-hao Xu Xiao-ming Zhang Hui-shun Lu |
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Institution: | (1) Department of Anesthesiology, Women’s Hospital, School of Medicine, Zhejiang University, Bachelor Road 1, Hangzhou, 310006, People’s Republic of China;(2) Institute of Anatomy and Cell Biology, School of Medicine, Zhejiang University, Hangzhou, China; |
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Abstract: | Emerging evidence has demonstrated that exposure to anesthetics early in life caused neurohistopathologic changes and persistent
behavioral impairments. In this study, a maternal fetal rat model was developed to study the effects of isoflurane exposure
during pregnancy on postnatal memory and learning in the offspring. Pregnant rats at gestational day 14 were either exposed
to 1.3% isoflurane in a humidified 100% oxygen carrier gas or simply humidified 100% oxygen without any inhalational anesthetic
for 2 h every day before delivery. Four weeks later, spatial learning and memory of the offspring were examined using the
Morris Water Maze. The expression levels of GAP-43 and NPY in the hippocampal CA1 region of the pups were determined by immunohistochemistry
and RT-PCR. Simultaneously, the ultrastructure changes in synapse of the hippocampus were also observed by transmission electron
microscopy (TEM). Isoflurane exposure during pregnancy impaired postnatal spatial memory and learning in the offspring as
shown by the longer escape latency and the fewer original platform crossings in the Morris Water Maze test. The number and
optical densities of GAP-43 and NPY positive cells, as well as the levels of GAP-43 and NPY mRNA, decreased significantly
in the hippocampus of isoflurane-exposed pups. Furthermore, TEM studies showed remarkable changes in synaptic ultrastructure
of hippocampus. These results indicate that isoflurane exposure during pregnancy could cause postnatal spatial memory and
learning impairments in offspring rats, which may be partially explained by the down-regulation of GAP-43 and NPY in the hippocampal
area. |
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