@article{ref1,
title="Characterization of the excitatory mechanism induced by Jingzhaotoxin-I inhibiting sodium channel inactivation",
journal="Toxicon: Journal of the International Society on Toxinology",
year="2007",
author="Xiao, Yucheng and Li, Jiang and Deng, Meichun and Dai, Changliang and Liang, Songping",
volume="50",
number="4",
pages="507-517",
abstract="We have recently isolated a peptide neurotoxin, Jingzhaotoxin-I (JZTX-I), from Chinese tarantula Chilobrachys jingzhao venom that preferentially inhibits cardiac sodium channel inactivation and may define a new subclass of spider sodium channel toxins. In this study, we found that in contrast to other spider sodium channel toxins acting presynaptically rather than postsynaptically, JZTX-I augmented frog end-plate potential amplitudes and caused an increase in both nerve mediated and unmediated muscle twitches. Although JZTX-I does not negatively shift sodium channel activation threshold, an evident increase in muscle fasciculation was detected. In adult rat dorsal root ganglion neurons JZTX-I (1 microM) induced a significant sustained tetrodotoxin-sensitive (TTX-S) current that did not decay completely during 500 ms and was inhibited by 0.1 microM TTX or depolarization due to voltage-dependent acceleration of toxin dissociation. Moreover, JZTX-I decreased closed-state inactivation and increased the rate of recovery of sodium channels, which led to an augmentation in TTX-S ramp currents and decreasing the amount of inactivation in a use-dependant manner. Together, these data suggest that JZTX-I acted both presynaptically and postsynaptically and facilitated the neurotransmitter release by biasing the activities of sodium channels towards open state. These actions are similar to those of scorpion alpha-toxin Lqh II.<p /><p>Language: en</p>",
language="en",
issn="0041-0101",
doi="10.1016/j.toxicon.2007.04.018",
url="http://dx.doi.org/10.1016/j.toxicon.2007.04.018"
}