TY - JOUR
T1 - Early-life midazolam exposure persistently changes chromatin accessibility to impair adult hippocampal neurogenesis and cognition
AU - Doi, Hiroyoshi
AU - Matsuda, Taito
AU - Sakai, Atsuhiko
AU - Matsubara, Shuzo
AU - Hoka, Sumio
AU - Yamaura, Ken
AU - Nakashima, Kinichi
N1 - Funding Information:
ACKNOWLEDGMENTS. We thank H. Nakashima, S. Katada, and T. Imamura for discussions and Y. Nakagawa for excellent secretarial assistance. We appreciate technical assistance from the Research Support Center, Research Center for Human Disease Modeling, Kyushu University Graduate School of Medical Sciences. This work was supported by Grants-in-Aid for Scientific Research on Innovative Areas JP16H06527 and JP16K21734 (to K.N.), a Grant-in-Aid for Young Scientists (B) JP18K14820 (to T.M.), a GSK Japan Research Grant 2017 (to T.M.), a Grant-in-Aid for Scientific Research (B) JP21H02808 (to T.M.), and a Research Grant for Public Health Science (to H.D.).
Publisher Copyright:
© 2021 National Academy of Sciences. All rights reserved.
PY - 2021/9/21
Y1 - 2021/9/21
N2 - Linkage between early-life exposure to anesthesia and subsequent learning disabilities is of great concern to children and their families. Here we show that early-life exposure to midazolam (MDZ), a widely used drug in pediatric anesthesia, persistently alters chromatin accessibility and the expression of quiescence-associated genes in neural stem cells (NSCs) in the mouse hippocampus. The alterations led to a sustained restriction of NSC proliferation toward adulthood, resulting in a reduction of neurogenesis that was associated with the impairment of hippocampal-dependent memory functions. Moreover, we found that voluntary exercise restored hippocampal neurogenesis, normalized the MDZ-perturbed transcriptome, and ameliorated cognitive ability in MDZ-exposed mice. Our findings thus explain how pediatric anesthesia provokes long-term adverse effects on brain function and provide a possible therapeutic strategy for countering them.
AB - Linkage between early-life exposure to anesthesia and subsequent learning disabilities is of great concern to children and their families. Here we show that early-life exposure to midazolam (MDZ), a widely used drug in pediatric anesthesia, persistently alters chromatin accessibility and the expression of quiescence-associated genes in neural stem cells (NSCs) in the mouse hippocampus. The alterations led to a sustained restriction of NSC proliferation toward adulthood, resulting in a reduction of neurogenesis that was associated with the impairment of hippocampal-dependent memory functions. Moreover, we found that voluntary exercise restored hippocampal neurogenesis, normalized the MDZ-perturbed transcriptome, and ameliorated cognitive ability in MDZ-exposed mice. Our findings thus explain how pediatric anesthesia provokes long-term adverse effects on brain function and provide a possible therapeutic strategy for countering them.
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U2 - 10.1073/pnas.2107596118
DO - 10.1073/pnas.2107596118
M3 - Article
C2 - 34526402
AN - SCOPUS:85115233642
SN - 0027-8424
VL - 118
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 38
M1 - e2107596118
ER -