Open AccessThe Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
Author(s) -
Amos Gdalyahu,
María Teresa Lázaro,
Olga Peñagarikano,
Peyman Golshani,
Joshua T. Trachtenberg,
Daniel H. Geschwind
Publication year - 2015
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0125633
Subject(s) - dendritic spine , neuroscience , autism , biology , in vivo , spine (molecular biology) , biological neural network , microbiology and biotechnology , psychology , genetics , hippocampal formation , developmental psychology
The establishment and maintenance of neuronal circuits depends on tight regulation of synaptic contacts. We hypothesized that CNTNAP2, a protein associated with autism, would play a key role in this process. Indeed, we found that new dendritic spines in mice lacking CNTNAP2 were formed at normal rates, but failed to stabilize. Notably, rates of spine elimination were unaltered, suggesting a specific role for CNTNAP2 in stabilizing new synaptic circuitry.