| First Author | Dachtler J | Year | 2015 |
| Journal | Behav Neurosci | Volume | 129 |
| Issue | 6 | Pages | 765-76 |
| PubMed ID | 26595880 | Mgi Jnum | J:250055 |
| Mgi Id | MGI:6101814 | Doi | 10.1037/bne0000108 |
| Citation | Dachtler J, et al. (2015) Heterozygous deletion of alpha-neurexin I or alpha-neurexin II results in behaviors relevant to autism and schizophrenia. Behav Neurosci 129(6):765-76 |
| abstractText | The neurexins are a family of presynaptic cell adhesion molecules. Human genetic studies have found heterozygous deletions affecting NRXN1 and NRXN2, encoding alpha-neurexin I (Nrxn1alpha) and alpha-neurexin II (Nrxn2alpha), in individuals with autism spectrum disorders and schizophrenia. However, the link between alpha-neurexin deficiency and the manifestation of psychiatric disorders remain unclear. To assess whether the heterozygous loss of neurexins results in behaviors relevant to autism or schizophrenia, we used mice with heterozygous (HET) deletion of Nrxn1alpha or Nrxn2alpha. We found that in a test of social approach, Nrxn1alpha HET mice show no social memory for familiar versus novel conspecifics. In a passive avoidance test, female Nrxn1alpha HET mice cross to the conditioned chamber sooner than female wild-type and Nrxn2alpha HET mice. Nrxn2alpha HET mice also express a lack of long-term object discrimination, indicating a deficit in cognition. The observed Nrxn1alpha and Nrxn2alpha genotypic effects were specific, as neither HET deletion had effects on a wide range of other behavioral measures, including several measures of anxiety. Our findings demonstrate that the heterozygous loss of alpha-neurexin I and alpha-neurexin II in mice leads to phenotypes relevant to autism and schizophrenia. |
