ArticleFrontiers in pharmacology2016
A Missense Mutation of the Gene Encoding Synaptic Vesicle Glycoprotein 2A (SV2A) Confers Seizure Susceptibility by Disrupting Amygdalar Synaptic GABA Release.
Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Sleep differentially modulates synaptic vesicle protein 2A and spine density across cortical regions and development.iScience · 2026Article
- Synaptic Vesicle Glycoprotein 2A Knockout in Parvalbumin and Somatostatin Interneurons Drives Seizures in the Postnatal Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Control of Synaptotagmin-1 Trafficking by SV2A-Mechanism and Consequences for Presynaptic Function and Dysfunction.Journal of neurochemistry · 2025Review
- Impact of levetiracetam and ethanol on memory, selected neurotransmitter levels, oxidative stress parameters, and essential elements in rats.Pharmacological reports : PR · 2024Article
- Synaptic vesicle protein 2A mitigates parthanatos via apoptosis-inducing factor in a rat model of pharmacoresistant epilepsy.CNS neuroscience & therapeutics · 2024Article
- Imbalance of glutamatergic and GABAergic neurotransmission in audiogenic seizure-susceptible LHeliyon · 2023Article
- Second Generation of Antiepileptic Drugs and Oxidative Stress.International journal of molecular sciences · 2023Review
- Levetiracetam Mechanisms of Action: From Molecules to Systems.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Synaptic Vesicle Glycoprotein 2A: Features and Functions.Frontiers in neuroscience · 2022Review
- Synaptopathies in Developmental and Epileptic Encephalopathies: A Focus on Pre-synaptic Dysfunction.Frontiers in neurology · 2022Review
- Synaptic Vesicle Protein 2A Expression in Glutamatergic Terminals Is Associated with the Response to Levetiracetam Treatment.Brain sciences · 2021Article
- An Epilepsy-Associated SV2A Mutation Disrupts Synaptotagmin-1 Expression and Activity-Dependent Trafficking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy?Epilepsia · 2020Review
- Synaptic vesicle protein 2: A multi-faceted regulator of secretion.Seminars in cell & developmental biology · 2019Review
- Puzzling Out Synaptic Vesicle 2 Family Members Functions.Frontiers in molecular neuroscience · 2017Review
- Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons.Frontiers in pharmacology · 2017Article
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9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic vesicle glycoprotein 2A (SV2A) is specifically expressed in the membranes of synaptic vesicles and modulates action potential-dependent neurotransmitter release. To explore the role of SV2A in the pathogenesis of epileptic disorders, we recently generated a novel rat model (Sv2a(L174Q) rat) carrying a missense mutation of the Sv2a gene and showed that the Sv2a(L174Q) rats were hypersensitive to kindling development (Tokudome et al., 2016). Here, we further conducted behavioral and neurochemical studies to clarify the pathophysiological mechanisms underlying the seizure vulnerability in Sv2a(L174Q) rats. Sv2a(L174Q) rats were highly susceptible to pentylenetetrazole (PTZ)-induced seizures, yielding a significantly higher seizure scores and seizure incidence than the control animals. Brain mapping analysis of Fos expression, a biological marker of neural excitation, revealed that the seizure threshold level of PTZ region-specifically elevated Fos expression in the amygdala in Sv2a(L174Q) rats. In vivo microdialysis study showed that the Sv2a(L174Q) mutation preferentially reduced high K(+) (depolarization)-evoked GABA release, but not glutamate release, in the amygdala. In addition, specific control of GABA release by SV2A was supported by its predominant expression in GABAergic neurons, which were co-stained with antibodies against SV2A and glutamate decarboxylase 1. The present results suggest that dysfunction of SV2A by the missense mutation elevates seizure susceptibility in rats by preferentially disrupting synaptic GABA release in the amygdala, illustrating the crucial role of amygdalar SV2A-GABAergic system in epileptogenesis.
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