Swimming exercise ameliorates neurocognitive impairment induced by neonatal exposure to isoflurane and enhances hippocampal histone acetylation in mice
Swimming exercise ameliorates neurocognitive impairment induced by neonatal exposure to isoflurane and enhances hippocampal histone acetylation in mice
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游泳运动可改善新生儿暴露于异氟烷引起的神经认知障碍，并增强小鼠海马组蛋白乙酰化
DOI：
10.1016/j.neuroscience.2015.12.049
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发表时间：
2016-03
期刊：
影响因子：
3.3
通讯作者：
Guo Q. L.
中科院分区：
文献类型：
--
作者：
Zhong T.;Ren F.;Huang C. S.;Zou W. Y.;Yang Y.;Pan Y. D.;Sun B.;Wang E.;Guo Q. L.
异氟烷诱导的啮齿动物大脑发育中的神经认知功能障碍有充分的记录，定期体育锻炼已被证明是一种可行的干预某些类型的神经认知功能障碍。本研究旨在探讨游泳运动对新生儿反复暴露于异氟醚引起的神经认知功能损害的潜在保护作用及其分子机制。小鼠在出生后第7、8和9天接受0.75%异氟烷暴露4小时。从麻醉后第三个月开始，小鼠进行4周的定期游泳运动，然后进行情境恐惧条件（CFC）试验。我们发现，反复暴露于异氟烷的新生儿减少冷冻行为CFC测试和去调节海马组蛋白H4 K12乙酰化。相反，经常游泳运动的小鼠海马H3 K9，H4 K5和H4 K12乙酰化水平增强，CFC训练后1小时c-Fos阳性细胞数量增加，异氟烷诱导的记忆障碍减少。我们还观察到组蛋白乙酰化和cAMP反应元件结合蛋白（CREB）结合蛋白（CBP）在游泳运动计划的增加。结果表明，新生儿异氟醚麻醉诱导的记忆障碍与H4 K12乙酰化的失调有关，这可能导致学习任务后海马激活减少。游泳运动与海马组蛋白乙酰化和CBP表达增强相关。运动很可能通过增强海马组蛋白乙酰化和在记忆形成过程中激活更多的神经元细胞来改善异氟醚诱导的记忆障碍。
Isoflurane-induced neurocognitive impairment in the developing rodent brain is well documented, and regular physical exercise has been demonstrated to be a viable intervention for some types of neurocognitive impairment. This study was designed to investigate the potential protective effect of swimming exercise on both neurocognitive impairment caused by repeated neonatal exposure to isoflurane and the underlying molecular mechanism. Mice received 0.75% isoflurane exposures for 4 h on postnatal days 7, 8, and 9. From the third month after anesthesia, the mice were subjected to regular swimming exercise for 4 weeks, followed by a contextual fear condition (CFC) trial. We found that repeated neonatal exposure to isoflurane reduced freezing behavior during CFC testing and deregulated hippocampal histone H4K12 acetylation. Conversely, mice subjected to regular swimming exercise showed enhanced hippocampal H3K9, H4K5, and H4K12 acetylation levels, increased numbers of c-Fos-positive cells 1 h after CFC training, and less isoflurane-induced memory impairment. We also observed increases in histone acetylation and of cAMP-response element-binding protein (CREB)-binding protein (CBP) during the swimming exercise program. The results suggest that neonatal isoflurane exposure-induced memory impairment was associated with dysregulation of H4K12 acetylation, which may lead to less hippocampal activation following learning tasks. Swimming exercise was associated with enhanced hippocampal histone acetylation and CBP expression. Exercise most likely ameliorated isoflurane-induced memory impairment by enhancing hippocampal histone acetylation and activating more neuron cells during memory formation.
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影响因子：
3.6
作者：
W. S. Almeida;L. C. J. Lima;V. N. Cunha;Rafael Rodrigues da Cunha;Ronaldo C. Araujo;Carlos Castilho Barros;Herbert Gustavo Simões;C. Campbell
通讯作者：
W. S. Almeida;L. C. J. Lima;V. N. Cunha;Rafael Rodrigues da Cunha;Ronaldo C. Araujo;Carlos Castilho Barros;Herbert Gustavo Simões;C. Campbell
DOI：
10.4049/jimmunol.0801892
发表时间：
2009-08-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Saha RN;Ghosh A;Palencia CA;Fung YK;Dudek SM;Pahan K
通讯作者：
Pahan K
影响因子：
5.3
作者：
Adlard, PA;Perreau, VM;Cotman, CW
通讯作者：
Cotman, CW
影响因子：
5.3
作者：
van Praag, H;Shubert, T;Gage, FH
通讯作者：
Gage, FH
DOI：
10.1073/pnas.1012851108
发表时间：
2010-12-28
影响因子：
11.1
作者：
Caccamo, Antonella;Maldonado, Monica A.;Oddo, Salvatore
通讯作者：
Oddo, Salvatore