• K T E Kleijer, A Zuko, Y Shimoda, K Watanabe, and J P H Burbach.
• Department of Translational Neuroscience, Brain Center Rudolf Magnus, UMC Utrecht, Stratenum 4.205, P.O. Box 85060, 3508 AB Utrecht, The Netherlands.
• Neuroscience. 2015 Dec 3;310:106-13.

AbstractThe gene encoding the neural cell adhesion molecule Cntn5 (a.k.a. NB-2) has been put forward as a candidate in neurodevelopmental disorders, like autism spectrum disorder (ASD), by recent genetic findings. Little is known about the expression pattern and function of the gene, and its functional involvement in brain development has remained elusive. So far, most research has focused on its early postnatal expression in the auditory system, where the absence of Cntn5 causes abnormal responses to acoustic stimuli and a decrease in fiber density. The current study shows that the Cntn5 gene is expressed in forebrain structures during embryonic development, starting at E15.5, and that it continues to be expressed into adulthood. Sites of strong expression included the thalamus, the caudate putamen (CPu) and to a lesser extent layer Va of the cerebral cortex. Cntn5-positive thalamic nuclei include the laterodorsal (LD), ventrolateral (VL) and posterior group (Po), which contain glutamatergic neurons. Visualization of the expression pattern through the Tau-LacZ fusion protein coded by an insert in the Cntn5 gene, demonstrated that Cntn5-positive nuclei of the thalamus project to the cortex, based on co-localization with thalamocortical markers L1 and Calretinin. These results indicate that the cell adhesion functions of Cntn5 are exploited for circuit formation and connectivity in early development and for synaptic maintenance during adulthood. Subtle alterations in the formation of the thalamocortical circuit may contribute to neurodevelopmental disorders, such as ASD.Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

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