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Mice lacking the synaptic adhesion molecule Neph2/Kirrel3 display moderate hyperactivity and defective novel object preference

Authors
Choi, Su-YeonHan, KihoonCutforth, TylerChung, WoosukPark, HaremLee, DongsooKim, RyunheeKim, Myeong-HeuiChoi, YeeunShen, KangKim, Eunjoon
Issue Date
28-7월-2015
Publisher
FRONTIERS MEDIA SA
Keywords
synaptic adhesion; intellectual disability; cognition; autism spectrum disorder; hyperactivity; memory; synaptic transmission
Citation
FRONTIERS IN CELLULAR NEUROSCIENCE, v.9
Indexed
SCIE
SCOPUS
Journal Title
FRONTIERS IN CELLULAR NEUROSCIENCE
Volume
9
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/92984
DOI
10.3389/fncel.2015.00283
ISSN
1662-5102
Abstract
Synaptic adhesion molecules regulate diverse aspects of neuronal synapse development, including synapse specificity, formation, and maturation. Neph2, also known as KirreI3, is an immunoglobulin superfamily adhesion molecule implicated in intellectual disability, neurocognitive delay associated with Jacobsen syndrome, and autism spectrum disorders. We here report mice lacking Neph2 (Neph2(-/-) mice) display moderate hyperactivity in a familiar, but not novel, environment and defective novel object recognition with normal performances in Morris water maze spatial learning and memory, contextual fear conditioning and extinction, and pattern separation tests. These mice also show normal levels of anxiety-like behaviors, social interaction, and repetitive behaviors. At the synapse level, Neph2(-/-) dentate gyrus granule cells exhibit unaltered dendritic spine density and spontaneous excitatory synaptic transmission. These results suggest that Neph2 is important for normal locomotor activity and object recognition memory.
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