Deficits in Tactile Learning in a Mouse Model of Fragile X Syndrome

被引:45
|
作者
Arnett, Megan T. [1 ]
Herman, David H. [2 ]
McGee, Aaron W. [1 ]
机构
[1] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles,Saban Res Inst, Dept Pediat,Dev Neurosci Program, Los Angeles, CA 90033 USA
[2] Univ So Calif, Dept Biol Sci, Neurobiol Sect, Los Angeles, CA 90089 USA
来源
PLOS ONE | 2014年 / 9卷 / 10期
关键词
PRIMARY SOMATOSENSORY CORTEX; FUNCTIONAL ARCHITECTURE; SYNAPTIC PLASTICITY; INTRINSIC SIGNAL; MICE; HYPEREXCITABILITY; TRANSLATION; INHIBITION; PHENOTYPE; AMYGDALA;
D O I
10.1371/journal.pone.0109116
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The fragile X mental retardation 1 mutant mouse (Fmr1 KO) recapitulates several of the neurologic deficits associated with Fragile X syndrome (FXS). As tactile hypersensitivity is a hallmark of FXS, we examined the sensory representation of individual whiskers in somatosensory barrel cortex of Fmr1 KO and wild-type (WT) mice and compared their performance in a whisker-dependent learning paradigm, the gap cross assay. Fmr1 KO mice exhibited elevated responses to stimulation of individual whiskers as measured by optical imaging of intrinsic signals. In the gap cross task, initial performance of Fmr1 KO mice was indistinguishable from WT controls. However, while WT mice improved significantly with experience at all gap distances, Fmr1 KO mice displayed significant and specific deficits in improvement at longer distances which rely solely on tactile information from whiskers. Thus, Fmr1 KO mice possess altered cortical responses to sensory input that correlates with a deficit in tactile learning.
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页数:7
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