ArticlePloS one2012
Lovastatin modulates glycogen synthase kinase-3β pathway and inhibits mossy fiber sprouting after pilocarpine-induced status epilepticus.
Article in PloS one, 2012. 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, 40 citations in OpenAlex.
- Wnt Signaling Modulators Exhibit Neuroprotective Effects via Combating Astrogliosis and Balancing Synaptic Density at Early and Late Stage Temporal Lobe Epilepsy.Neurochemical research · 2024Article
- Autophagy and autophagy signaling in Epilepsy: possible role of autophagy activator.Molecular medicine (Cambridge, Mass.) · 2023Review
- Scoping review of disease-modifying effect of drugs in experimental epilepsy.Frontiers in neurology · 2023Article
- Beneficial Effects of Statins on Seizures Independent of Their Lipid-Lowering Effect: A Narrative Review.Iranian journal of medical sciences · 2023Review
- Brain glycogen content is increased in the acute and interictal chronic stages of the mouse pilocarpine model of epilepsy.Epilepsia open · 2022Article
- Effects of atorvastatin and metformin on development of pentylenetetrazole-induced seizure in mice.Heliyon · 2020Article
- GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy.Frontiers in cellular neuroscience · 2020Article
- Neuroprotective effects of lovastatin in the pilocarpine rat model of epilepsy according to the expression of neurotrophic factors.Metabolic brain disease · 2019Article
- GSK3β activity alleviates epileptogenesis and limits GluA1 phosphorylation.EBioMedicine · 2019Article
- GSK-3Neural plasticity · 2019Review
- Bi-directional genetic modulation of GSK-3β exacerbates hippocampal neuropathology in experimental status epilepticus.Cell death & disease · 2018Article
- PI3K-mTOR-S6K Signaling Mediates Neuronal Viability via Collapsin Response Mediator Protein-2 Expression.Frontiers in molecular neuroscience · 2017Article
- Specific binding of lacosamide to collapsin response mediator protein 2 (CRMP2) and direct impairment of its canonical function: implications for the therapeutic potential of lacosamide.Molecular neurobiology · 2015Review
- Molecular and clinical aspects of drug-induced gingival overgrowth.Journal of dental research · 2015Review
- The potential of antiseizure drugs and agents that act on novel molecular targets as antiepileptogenic treatments.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Review
- Article
- Differential regulation of collapsin response mediator protein 2 (CRMP2) phosphorylation by GSK3ß and CDK5 following traumatic brain injury.Frontiers in cellular neuroscience · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was undertaken to assay the effect of lovastatin on the glycogen synthase kinase-3 beta (GSK-3β) and collapsin responsive mediator protein-2 (CRMP-2) signaling pathway and mossy fiber sprouting (MFS) in epileptic rats. MFS in the dentate gyrus (DG) is an important feature of temporal lobe epilepsy (TLE) and is highly related to the severity and the frequency of spontaneous recurrent seizures. However, the molecular mechanism of MFS is mostly unknown. GSK-3β and CRMP-2 are the genes responsible for axonal growth and neuronal polarity in the hippocampus, therefore this pathway is a potential target to investigate MFS. Pilocarpine-induced status epilepticus animal model was taken as our researching material. Western blot, histological and electrophysiological techniques were used as the studying tools. The results showed that the expression level of GSK-3β and CRMP-2 were elevated after seizure induction, and the administration of lovastatin reversed this effect and significantly reduced the extent of MFS in both DG and CA3 region in the hippocampus. The alteration of expression level of GSK-3β and CRMP-2 after seizure induction proposes that GSK-3β and CRMP-2 are crucial for MFS and epiletogenesis. The fact that lovastatin reversed the expression level of GSK-3β and CRMP-2 indicated that GSK-3β and CRMP-2 are possible to be a novel mechanism of lovatstain to suppress MFS and revealed a new therapeutic target and researching direction for studying the mechanism of MFS and epileptogenesis.
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