ArticleCNS neuroscience & therapeutics2020
Atlastin-1 modulates seizure activity and neuronal excitability.
Article in CNS neuroscience & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Connecting tubules: mechanisms of endoplasmic reticulum membrane fusion.Biochemical Society transactions · 2025Review
- Review
- Atlastin-1 modulates seizure activity and neuronal excitability.CNS neuroscience & therapeutics · 2020Article
- Dynamic Transitions in Neuronal Network Firing Sustained by Abnormal Astrocyte Feedback.Neural plasticity · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is a neurological disease, and the main clinical manifestation is recurrent seizures. The exact etiology of epilepsy and the pathogenesis of the disorder are not yet fully understood. Atlastin-1, a dynamin-like GTPase, interacts with microtubules and is responsible for vesicle formation, both of which are highly associated with the development of epilepsy. Here, we reported that the expression level of atlastin-1 protein was reduced in the temporal neocortex of patients with temporal lobe epilepsy and in the hippocampus and adjacent cortex of a pentylenetetrazol-kindled epileptic mouse model. Cells expressing atlastin-1 coexpressed the inhibitory synaptic marker GAD67 in the temporal cortex and hippocampus of patients with epilepsy and an epileptic mouse model. The lentivirus-mediated overexpression of atlastin-1 protein in the hippocampus of mice suppressed seizure activity in behavioral experiments. Patch-clamp recordings in the Mg
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Registered trials
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