Structural abnormalities in the primary somatosensory cortex and a normal behavioral profile in Contactin-5 deficient mice

Cell Adh Migr. 2018 Jan 2;12(1):5-18. doi: 10.1080/19336918.2017.1288788. Epub 2017 Mar 27.

Abstract

Contactin-5 (Cntn5) is an immunoglobulin cell adhesion molecule that is exclusively expressed in the central nervous system. In view of its association with neurodevelopmental disorders, particularly autism spectrum disorder (ASD), this study focused on Cntn5-positive areas in the forebrain and aimed to explore the morphological and behavioral phenotypes of the Cntn5 null mutant (Cntn5-/-) mouse in relation to these areas and ASD symptomatology. A newly generated antibody enabled us to elaborately describe the spatial expression pattern of Cntn5 in P7 wild type (Cntn5+/+) mice. The Cntn5 expression pattern included strong expression in the cerebral cortex, hippocampus and mammillary bodies in addition to described previously brain nuclei of the auditory pathway and the dorsal thalamus. Thinning of the primary somatosensory (S1) cortex was found in Cntn5-/- mice and ascribed to a misplacement of Cntn5-ablated cells. This phenotype was accompanied by a reduction in the barrel/septa ratio of the S1 barrel field. The structure and morphology of the hippocampus was intact in Cntn5-/- mice. A set of behavioral experiments including social, exploratory and repetitive behaviors showed that these were unaffected in Cntn5-/- mice. Taken together, these data demonstrate a selective role of Cntn5 in development of the cerebral cortex without overt behavioral phenotypes.

Keywords: autism spectrum disorder; behavior; contactin-5; hippocampus; primary somatosensory cortex.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autism Spectrum Disorder / genetics
  • Autism Spectrum Disorder / pathology
  • Behavior, Animal / physiology*
  • Cerebral Cortex / growth & development*
  • Contactins / deficiency*
  • Contactins / metabolism
  • Hippocampus / pathology
  • Mice, Knockout
  • Nerve Tissue Proteins / metabolism
  • Somatosensory Cortex / abnormalities*

Substances

  • Cntn5 protein, mouse
  • Contactins
  • Nerve Tissue Proteins

Grants and funding

This study was supported by Innovative Medicines Initiative Joint Undertaking under Grant Agreement No. 115300 (EU-AIMS), resources of which are composed of financial contribution from the European Union's Seventh Framework Program (FP7/2007–2013) and EFPIA companies' in kind contribution.