ArticleNeural plasticity2014
Downregulated GABA and BDNF-TrkB pathway in chronic cyclothiazide seizure model.
Article in Neural plasticity, 2014. 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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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Preclinical characterization of a water-soluble low-impact ampakine prodrug, CX1942 and its active moiety, CX1763.Future medicinal chemistry · 2024Article
- Preclinical Pharmacology of CX1837, a High-Impact Ampakine with an Improved Safety Margin: Implications for Treating Alzheimer's Disease and Ischemic Stroke.Current Alzheimer research · 2024Article
- Furosemide prevents membrane KCC2 downregulation during convulsant stimulation in the hippocampus.IBRO neuroscience reports · 2022Article
- The Anticonvulsant Effects of Baldrinal on Pilocarpine-Induced convulsion in Adult Male Mice.Molecules (Basel, Switzerland) · 2019Article
- Protective Role of L-3-Frontiers in pharmacology · 2018Article
- Brain-derived neurotropic factor and GABAergic transmission in neurodegeneration and neuroregeneration.Neural regeneration research · 2017Review
- Chloride Co-transporter NKCC1 Inhibitor Bumetanide Enhances Neurogenesis and Behavioral Recovery in Rats After Experimental Stroke.Molecular neurobiology · 2017Article
- CXCR4 Antagonist AMD3100 Suppresses the Long-Term Abnormal Structural Changes of Newborn Neurons in the Intraventricular Kainic Acid Model of Epilepsy.Molecular neurobiology · 2016Article
- BDNF-TrkB pathway mediates neuroprotection of hydrogen sulfide against formaldehyde-induced toxicity to PC12 cells.PloS one · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclothiazide (CTZ) has been reported to simultaneously enhance glutamate receptor excitation and inhibit GABAA receptor inhibition, and in turn it evokes epileptiform activities in hippocampal neurons. It has also been shown to acutely induce epileptic seizure behavior in freely moving rats. However, whether CTZ induced seizure rats could develop to have recurrent seizure still remains unknown. In the current study, we demonstrated that 46% of the CTZ induced seizure rats developed to have recurrent seizure behavior as well as epileptic EEG with a starting latency between 2 weeks and several months. In those chronic seizure rats 6 months after the seizure induction by the CTZ, our immunohistochemistry results showed that both GAD and GAT-1 were significantly decreased across CA1, CA3, and dentate gyrus area of the hippocampus studied. In addition, both BDNF and its receptor TrkB were also decreased in hippocampus of the chronic CTZ seizure rats. Our results indicate that CTZ induced seizure is capable of developing to have recurrent seizure, and the decreased GABA synthesis and transport as well as the impaired BDNF-TrkB signaling pathway may contribute to the development of the recurrent seizure. Thus, CTZ seizure rats may provide a novel animal model for epilepsy study and anticonvulsant drug testing in the future.
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