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Altered dynamics of the cortical neuronal circuit in a mouse model of<br />
autism<br />
Shinji Tanaka 1 , Toru Takumi 2 , Shigeo Okabe 1<br />
1<br />
Department of Cellular Neurobiology, Graduate School of Medicine, University<br />
of Tokyo, 2 Laboratory of Integrative Bioscience, Graduate School of Biomedical<br />
Sciences, Hiroshima University<br />
Autism spectral disorder ASD is an early onset mental disease with impairments<br />
in higher cognitive functions. ASD symptoms may originate from altered<br />
connectivity of the neocortical neurons. This possibility can be tested by<br />
combining techniques of synapse imaging with reliable animal models of ASD.<br />
Genetically engineered mice that mimic the most frequent copy number variation<br />
in ASD human 15q1113 show multiple deficits in social behaviors. The<br />
postnatal synapse formation in the neocortex of this ASD model was studied by<br />
using twophoton in vivo imaging of pyramidal neurons expressing fluorescent<br />
proteins. Pyramidal neurons showed excess formation of nascent spines and<br />
their balanced elimination. Unexpectedly, analysis of PSD size changes in<br />
established spines, estimated from PSD95 clustering, revealed reduced PSD<br />
remodeling. Enhanced gain and loss of spines during network formation may<br />
increase mismatched connectivity, leading to altered pattern of neuronal activity<br />
that secondarily suppresses PSD remodeling. Negative correlation between<br />
spinogenesis and PSD remodeling may be a unique feature of this mouse model<br />
and its relevance to the etiology of ASD should be clarified.