The autism spectrum disorder risk gene NEXMIF alters hippocampal CA1 cellular and network dynamics
Mount, R. A.; Athif, M.; O'Connor, M.; Saligrama, A.; Tseng, H.-a.; Sridhar, S.; Zhou, C.; Man, H.; Han, X.
Show abstract
Perturbations in autism spectrum disorder (ASD) risk genes disrupt neural circuit dynamics and ultimately lead to behavioral abnormalities. To understand how ASD-implicated genes influence network computation during behavior, we performed in vivo calcium imaging from hundreds of individual hippocampal CA1 neurons simultaneously in freely locomoting mice with total knockout of NEXMIF. NEXMIF is an ASD risk gene most highly expressed in the hippocampus, and NEXMIF knockout in mice creates a range of behavioral deficits, including impaired hippocampal-dependent memory. We found that NEXMIF knockout does not alter the overall excitability of individual neurons but exaggerates movement-mediated neuronal responses. At the network level, NEXMIF knockout creates over-synchronization of the CA1 circuit, quantified by pairwise correlation and network closeness centrality. These neuronal effects observed upon NEXMIF knockout highlight the network consequences of perturbations in ASD-implicated genes, which have broad implications for cognitive performance and other ASD-related behavioral disruptions.
Matching journals
The top 4 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Optogenetic frequency scrambling of hippocampal theta oscillations dissociates working memory retrieval from hippocampal spatiotemporal codes 97%
- Ketamine evoked disruption of entorhinal and hippocampal spatial maps 97%
- Ketamine disinhibits dendrites and enhances calcium signals in prefrontal dendritic spines 97%
Similar papers in this journal
Similar papers in this journal
Similar papers in this journal
- The olivocerebellar system differentially encodes the effect sensory events exert on behavior 97%
- Perpetual step-like restructuring of hippocampal circuit dynamics 96%
- Ca2+-phospholipid-dependent regulation of Munc13-1 is essential for post-tetanic potentiation at mossy fiber synapses and supports working memory 96%
Similar papers in this journal
- Synchronicity in zebrafish locomotive circuit development mediated by electrical pacemaker interneurons 96%
- Visual recognition is heralded by shifts in local field potential oscillations and inhibitory networks in primary visual cortex 96%
- A pathogenic missense mutation in kainate receptors elevates dendritic excitability and synaptic integration through dysregulation of SK channels 96%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.