| First Author | Hammer M | Year | 2015 |
| Journal | Cell Rep | Volume | 13 |
| Issue | 3 | Pages | 516-523 |
| PubMed ID | 26456829 | Mgi Jnum | J:262682 |
| Mgi Id | MGI:6161871 | Doi | 10.1016/j.celrep.2015.09.011 |
| Citation | Hammer M, et al. (2015) Perturbed Hippocampal Synaptic Inhibition and gamma-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism. Cell Rep 13(3):516-523 |
| abstractText | Loss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are among the most common genetic abnormalities associated with autism spectrum disorders, but little is known about the function of Neuroligin-4 and the consequences of its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout mice, focusing on the hippocampus as a model brain region with a critical role in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects of the protein composition and function of GABAergic synapses in the hippocampal CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced perturbations of gamma-oscillatory network activity, which has been implicated in cognitive function and is altered in multiple psychiatric and neurodevelopmental disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent GABAergic synapses may contribute to autism phenotypes and indicate new strategies for therapeutic approaches. |
