| First Author | Hosseini S | Year | 2020 |
| Journal | Cell Rep | Volume | 31 |
| Issue | 7 | Pages | 107666 |
| PubMed ID | 32433975 | Mgi Jnum | J:300784 |
| Mgi Id | MGI:6488926 | Doi | 10.1016/j.celrep.2020.107666 |
| Citation | Hosseini S, et al. (2020) Type I Interferon Receptor Signaling in Astrocytes Regulates Hippocampal Synaptic Plasticity and Cognitive Function of the Healthy CNS. Cell Rep 31(7):107666 |
| abstractText | Type I interferon receptor (IFNAR) signaling is a hallmark of viral control and host protection. Here, we show that, in the hippocampus of healthy IFNAR-deficient mice, synapse number and synaptic plasticity, as well as spatial learning, are impaired. This is also the case for IFN-beta-deficient animals. Moreover, antibody-mediated IFNAR blocking acutely interferes with neuronal plasticity, whereas a low-dose application of IFN-beta has a positive effect on dendritic spine structure. Interfering with IFNAR signaling in different cell types shows a role for cognitive function and synaptic plasticity specifically mediated by astrocytes. Intriguingly, levels of the astrocytic glutamate-aspartate transporter (GLAST) are reduced significantly upon IFN-beta treatment and increase following inhibition of IFNAR signaling. These results indicate that, besides the prominent role for host defense, IFNAR is important for synaptic plasticity as well as cognitive function. Astrocytes are at the center stage of this so-far-unknown signaling cascade. |
