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Characterization of Functional Effects of Two New Active Fractions Isolated From Scorpion Venom on Neuronal Ca(2+) Spikes: A Possible Action on Ca(2+)-Dependent Dependent K(+) Channels

INTRODUCTION: It is a long time that natural toxin research is conducted to unlock the medical potential of toxins. Although venoms-toxins cause pathophysiological conditions, they may be effective to treat several diseases. Since toxins including scorpion toxins target voltage-gated ion channels, t...

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Detalles Bibliográficos
Autores principales: Tamadon, Hanieh, Ghasemi, Zahra, Ghasemi, Fatemeh, Hosseinmardi, Narges, Vatanpour, Hossein, Janahmadi, Mahyar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Iranian Neuroscience Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6484188/
https://www.ncbi.nlm.nih.gov/pubmed/31031893
http://dx.doi.org/10.32598/bcn.9.10.352
Descripción
Sumario:INTRODUCTION: It is a long time that natural toxin research is conducted to unlock the medical potential of toxins. Although venoms-toxins cause pathophysiological conditions, they may be effective to treat several diseases. Since toxins including scorpion toxins target voltage-gated ion channels, they may have profound effects on excitable cells. Therefore, elucidating the cellular and electrophysiological impacts of toxins, particularly scorpion toxins would be helpful in future drug development opportunities. METHODS: Intracellular recording was made from F1 cells of Helix aspersa in the presence of calcium Ringer solution in which Na(+) and K(+) channels were blocked. Then, the modulation of channel function in the presence of extracellular application of F4 and F6 toxins and kaliotoxin (KTX; 50 nM and 1 μM) was examined by assessing the electrophysiological characteristics of calcium spikes. RESULTS: The two active toxin fractions, similar to KTX, a known Ca(2+)-activated K(+) channel blocker, reduced the amplitude of AHP, enhanced the firing frequency of calcium spikes and broadened the duration of Ca(2+) spikes. Therefore, it might be inferred that these two new fractions induce neuronal hyperexcitability possibly, in part, by blocking calcium-activated potassium channel current. However, this supposition requires further investigation using voltage clamping technique. CONCLUSION: These toxin fractions may act as blocker of calcium-activated potassium channels.