Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
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-β-deficient animals. Moreover, antibody-mediated IFNAR blocking acutely interferes with neuronal plasticity, whereas a low-dose application of IFN-β 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-β 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.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.celrep.2020.107666 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
TRPV1 Suppresses Microglial Inflammatory Activation to Ameliorate Schizophrenia-Associated Behaviors in Maternal Separation Rats.
Schizophr Bull
September 2025
Department of Psychiatry, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Background And Hypothesis: Schizophrenia is linked to hippocampal dysfunction and microglial inflammatory activation. Our prior clinical findings revealed significantly reduced transient receptor potential vanilloid 1 (TRPV1) expression in both first-episode and recurrent schizophrenia patients, with levels inversely correlating with symptom severity, implicating TRPV1 dysfunction in disease progression. Preclinical maternal separation (MS) models recapitulate schizophrenia-like behavioral and synaptic deficits, paralleled by hippocampal microglial TRPV1 downregulation.
View Article and Find Full Text PDFLong-Term Treadmill Exercise and Voluntary Running Pre-Training Attenuates Vascular Dementia-Related Pathology by Regulating Hippocampal Structural Synaptic Plasticity in a Rat Model.
Brain Behav
September 2025
School of Physical Education and Health, Henan University of Chinese Medicine, Zhengzhou, China.
Background: Clinical and basic research suggests that exercise is a safe behavioral intervention and effective in improving cognition in vascular dementia (VD). However, despite global efforts, there is still no effective method to completely cure VD. This study aimed to investigate the effects of long-term exercise pretreatment on typical VD pathology in a rat model, and further compare the neuroprotective impacts of different exercise modalities on VD rats.
View Article and Find Full Text PDFStabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer's disease mouse model.
Acta Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
View Article and Find Full Text PDFAutophagy controls the hippocampal postsynaptic organization and affects cognition in a mouse model of Fragile X syndrome.
Mol Psychiatry
September 2025
Center for Gene Regulation in Health and Disease, Cleveland State University, Cleveland, OH, 44115, USA.
Dysregulated spine morphology is a common feature in the pathology of many neurodevelopmental and neuropsychiatric disorders. Overabundant immature dendritic spines in the hippocampus are causally related to cognitive deficits of Fragile X syndrome (FXS), the most common form of heritable intellectual disability. Recent findings from us and others indicate autophagy plays important roles in synaptic stability and morphology, and autophagy is downregulated in FXS neurons.
View Article and Find Full Text PDFLactylation as a metabolic-epigenetic nexus in epilepsy: Mechanisms and therapeutic implications.
Neurobiol Dis
September 2025
Department of Neurology, The Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi 563000, Guizhou, PR China; Key Laboratory of Brain Function and Brain Disease Prevention and Treatment of Guizhou Province, Zunyi 563000, Guizhou, PR China; The Collaborative Innovation Center of Tis
Lactylation is a novel post-translational modification (PTM) mediated by lactate, which dynamically regulates protein functions and gene expression by covalently attaching lactate groups to lysine residues. Recent studies have shown that abnormal lactate metabolism not only contributes to the pathogenesis of epilepsy through microenvironment acidification but also influences neuroinflammation, energy metabolism imbalance, neurotransmitter dysregulation, synaptic plasticity, and epigenetic regulation via lactylation. This positions lactylation as a critical metabolic-epigenetic intersection in the pathological mechanisms of epilepsy.
View Article and Find Full Text PDF