期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 114, 期 34, 页码 9188-9193出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1706069114
关键词
miR-9; learning; memory; Diap1; dendritogenesis
资金
- NIH [U54HD087101-02]
- Basic Research Program of China [2012CB966303, 2014CB964602, 31471009]
- Richard Heyler Award
- Brain & Behavior Research Foundation NARSAD Young Investigator Grant
- Australian Research Council Discovery Early Career Researcher Award (DECRA) [DE170100112]
- NIH/National Institute of Mental Health (NIMH) Grant [R01MH084095]
- Chinese National Natural Science Foundation [31271371, 91319309, 2016YFA0100801, 31620103904]
- NIMH [R01MH62122]
- Australian National Health and Medical Research Council [GNT1069570]
- Australian Research Council [DE170100112] Funding Source: Australian Research Council
The prenatal period of cortical development is important for the establishment of neural circuitry and functional connectivity of the brain; however, the molecular mechanisms underlying this process remain unclear. Here we report that disruption of the actin-cytoskeletal network in the developing mouse prefrontal cortex alters dendritic morphogenesis and synapse formation, leading to enhanced formation of fear-related memory in adulthood. These effects are mediated by a brain-enriched microRNA, miR-9, through its negative regulation of diaphanous homologous protein 1 (Diap1), a key organizer of the actin cytoskeletal assembly. Our findings not only revealed important regulation of dendritogenesis and synaptogenesis during early brain development but also demonstrated a tight link between these early developmental events and cognitive functions later in life.
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