期刊
FRONTIERS IN CELLULAR NEUROSCIENCE
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fncel.2018.00084
关键词
DPP6; neurodevelopment; learning and memory; autism spectrum disorder
资金
- Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development
- Intramural Research Program of NIH/National Institute on Deafness and Other Communication Disorders (NIDCD) [ZIC DC000081]
- Intramural Research Program of NIH/National Institute of Mental Health (NIMH)
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [ZIAHD008755] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [ZIAMH002784] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS [ZICDC000081] Funding Source: NIH RePORTER
DPP6 is well known as an auxiliary subunit of Kv4-containing, A-type K+ channels which regulate dendritic excitability in hippocampal CA1 pyramidal neurons. We have recently reported, however, a novel role for DPP6 in regulating dendritic filopodia formation and stability, affecting synaptic development and function. These results are notable considering recent clinical findings associating DPP6 with neurodevelopmental and intellectual disorders. Here we assessed the behavioral consequences of DPP6 loss. We found that DPP6 knockout (DPP6-KO) mice are impaired in hippocampus-dependent learning and memory. Results from the Morris water maze and T-maze tasks showed that DPP6-KO mice exhibit slower learning and reduced memory performance. DPP6 mouse brain weight is reduced throughout development compared with WT, and in vitro imaging results indicated that DPP6 loss affects synaptic structure and motility. Taken together, these results show impaired synaptic development along with spatial learning and memory deficiencies in DPP6-KO mice.
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