ArticleEpilepsy research2019
Calpain-dependent cleavage of GABAergic proteins during epileptogenesis.
Article in Epilepsy research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Pathogenic variants at the N-terminal arginine residue 44 disrupt human GABA transporter 1 function: insights fromFrontiers in pharmacology · 2025Article
- Inhibition of Calpain Attenuates Degeneration of Substantia Nigra Neurons in the Rotenone Rat Model of Parkinson's Disease.International journal of molecular sciences · 2022Article
- Regulation of Inhibitory Signaling at the Receptor and Cellular Level; Advances in Our Understanding of GABAergic Neurotransmission and the Mechanisms by Which It Is Disrupted in Epilepsy.Frontiers in synaptic neuroscience · 2022Review
- Stepwise disassembly of GABAergic synapses during pathogenic excitotoxicity.Cell reports · 2021Article
- Phosphorylation of Serine 157 Protects the Rat Glycine Transporter GlyT2 from Calpain Cleavage.Journal of molecular neuroscience : MN · 2020Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Epileptogenesis is the processes by which a normal brain transforms and becomes capable of generate spontaneous seizures. In acquired epilepsy, it is thought that epileptogenesis can be triggered by a brain injury but the understanding of the cellular or molecular changes unraveling is incomplete. In the CA1 region of hippocampus less GABAergic activity precede the appearance of spontaneous seizures and calpain overactivation has been detected after chemoconvulsant-induced status epilepticus (SE). Inhibition of calpain overactivation following SE ameliorates seizure burden, suggesting a role for calpain dysregulation in epileptogenesis. The current study analyzed if GABAergic proteins (i.e., gephyrin, the vesicular GABA transporter and the potassium chloride co-transporter 2) undergo calpain-dependent cleavage during epileptogenesis. A time-dependent generation of break down products (BDPs) for these proteins was observed in the CA1 region of hippocampus after pilocarpine-induced SE. Generation of these BDPs was partially blocked by treatment with the calpain inhibitor MDL-28170. These findings suggest that calpain-dependent loss of GABAergic proteins might promote the erosion of inhibitory drive and contribute to hyperexcitability during epileptogenesis.
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