ArticleScientific reports2021
The actin binding protein drebrin helps to protect against the development of seizure-like events in the entorhinal cortex.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 10 citations in OpenAlex.
- Forkhead box versus NF-κB hippocampal snRNA-seq profiles distinguish anti-Drebrin- and anti-GAD65-positive encephalitis.Journal of neuroinflammation · 2026Article
- Phosphoprofile reorganization of the actin binding protein Drebrin during long term depression.Frontiers in molecular neuroscience · 2025Article
- Autism spectrum disorder related phenotypes in a mouse model lacking the neuronal actin binding protein profilin 2.Frontiers in cellular neuroscience · 2025Article
- Unleashing the potential: 40 Hz multisensory stimulation therapy for cognitive impairment.Journal of central nervous system disease · 2025Review
- Vitamin D binding protein in psychiatric and neurological disorders: Implications for diagnosis and treatment.Genes & diseases · 2024Review
- A lack of drebrin causes olfactory impairment.Brain and behavior · 2024Article
- Sex-specific effects of subchronic NMDA receptor antagonist MK-801 treatment on hippocampal gamma oscillations.Frontiers in neuroscience · 2024Article
- Metabolic implications of axonal demyelination and its consequences for synchronized network activity: AnJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- The role of dendritic spines in epileptogenesis.Frontiers in cellular neuroscience · 2023Review
- Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability.Frontiers in neural circuits · 2021Article
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4 authors at 1 institution in 1 country.
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Abstract
The actin binding protein drebrin plays a key role in dendritic spine formation and synaptic plasticity. Decreased drebrin protein levels have been observed in temporal lobe epilepsy, suggesting the involvement of drebrin in the disease. Here we investigated the effect of drebrin knockout on physiological and pathophysiological neuronal network activities in mice by inducing gamma oscillations, involved in higher cognitive functions, and by analyzing pathophysiological epileptiform activity. We found that loss of drebrin increased the emergence of spontaneous gamma oscillations suggesting an increase in neuronal excitability when drebrin is absent. Further analysis showed that although the kainate-induced hippocampal gamma oscillations were unchanged in drebrin deficient mice, seizure like events measured in the entorhinal cortex appeared earlier and more frequently. The results suggest that while drebrin is not essential for normal physiological network activity, it helps to protect against the formation of seizure like activities during pathological conditions. The data indicate that targeting drebrin function could potentially be a preventive or therapeutic strategy for epilepsy treatment.
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