ArticleBritish journal of pharmacology2008
Anticonvulsant effect of BmK IT2, a sodium channel-specific neurotoxin, in rat models of epilepsy.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 33 citations in OpenAlex.
- The underlying mechanism of scorpion venom peptide BmK AS in reducing epilepsy seizures: mediated through dual modulation of Nav1.6 and the inflammasome pathway.Frontiers in pharmacology · 2026Article
- Scorpion (Buthus martensii Karsch) in Chinese medicine: a review of traditional uses, chemical constituents, pharmacology, and toxicology.Frontiers in pharmacology · 2025Review
- Molecular Genetics of Acquired Temporal Lobe Epilepsy.Biomolecules · 2024Review
- P/Q type (CaMolecular neurobiology · 2024Article
- Animal Venoms as Potential Source of Anticonvulsants.F1000Research · 2024Review
- A new class of peptides from wasp venom: a pathway to antiepileptic/neuroprotective drugs.Brain communications · 2023Article
- Scorpion venom peptide HsTx2 suppressed PTZ-induced seizures in mice via the circ_0001293/miR-8114/TGF-β2 axis.Journal of neuroinflammation · 2022Article
- Anticonvulsant Effects of Dingxian Pill in Pentylenetetrazol-Kindled Rats.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- A mutant of theThe Journal of biological chemistry · 2017Article
- Anticonvulsant Effects of Fractions Isolated from Dinoponera quadriceps (Kempt) Ant Venom (Formicidae: Ponerinae).Toxins · 2016Article
- Pro- and Anticonvulsant Effects of the Ant Dinoponera quadriceps (Kempf) Venom in Mice.Neotropical entomology · 2015Article
- Neuroactive compounds obtained from arthropod venoms as new therapeutic platforms for the treatment of neurological disorders.The journal of venomous animals and toxins including tropical diseases · 2015Article
- Scorpion ethanol extract and valproic acid effects on hippocampal glial fibrillary acidic protein expression in a rat model of chronic-kindling epilepsy induced by lithium chloride-pilocarpine.Neural regeneration research · 2012Article
- Localization of receptor site on insect sodium channel for depressant β-toxin BmK IT2.PloS one · 2011Article
- Cyclothiazide induces seizure behavior in freely moving rats.Brain research · 2010Article
- The Effects of the Fraction Isolated from IranianIranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe sodium channel is a primary target for treating central nervous system disorders such as epilepsy. In this study the anticonvulsant effect of BmK IT2, a sodium channel-specific neurotoxin, was evaluated in different animal models of epilepsy. EXPERIMENTAL APPROACH: Experiments were performed on freely moving rats made epileptic by administration of either pentylenetetrazole (PTZ) or pilocarpine. BmK IT2 (0.05-0.5 microg in 2 microl) was microinjected into the CA1 area and its effects on PTZ-induced widespread, seizure-like behaviour and cortex epileptiform EEG, as well as on pilocarpine-induced seizure-like behaviour and c-Fos expression were studied. KEY
resultsIntrahippocampal application of BmK IT2 dose-dependently inhibited PTZ-induced seizure-like behaviour, and reduced the numbers and duration of the high amplitude and frequency discharges (HAFDs) of the epileptiform EEG component induced by PTZ. Similarly, in the pilocarpine-induced status epilepticus (SE) model, BmK IT2 significantly prolonged the latency to onset of the SE, reduced the severity of SE and suppressed hippocampal c-Fos expression during SE. CONCLUSIONS AND IMPLICATIONS: BmK IT2 showed anticonvulsant activity as it inhibited the widespread seizures induced by PTZ and pilocarpine-induced SE in rats. This activity might be due to the modulation of sodium channels in the hippocampus. Hence, BmK IT2 could be used as a novel tool to explore the molecular and pathological mechanisms of epilepsy with regard to the involvement of sodium channels.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.