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Characterization of the excitatory mechanism induced by Jingzhaotoxin-I inhibiting sodium channel inactivation.
Toxicon. 2007 Sep 15; 50(4):507-17.T

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.

Authors+Show Affiliations

Life Sciences College, Hunan Normal University, Changsha, Hunan 410081, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17618665

Citation

Xiao, Yucheng, et al. "Characterization of the Excitatory Mechanism Induced By Jingzhaotoxin-I Inhibiting Sodium Channel Inactivation." Toxicon : Official Journal of the International Society On Toxinology, vol. 50, no. 4, 2007, pp. 507-17.
Xiao Y, Li J, Deng M, et al. Characterization of the excitatory mechanism induced by Jingzhaotoxin-I inhibiting sodium channel inactivation. Toxicon. 2007;50(4):507-17.
Xiao, Y., Li, J., Deng, M., Dai, C., & Liang, S. (2007). Characterization of the excitatory mechanism induced by Jingzhaotoxin-I inhibiting sodium channel inactivation. Toxicon : Official Journal of the International Society On Toxinology, 50(4), 507-17.
Xiao Y, et al. Characterization of the Excitatory Mechanism Induced By Jingzhaotoxin-I Inhibiting Sodium Channel Inactivation. Toxicon. 2007 Sep 15;50(4):507-17. PubMed PMID: 17618665.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Characterization of the excitatory mechanism induced by Jingzhaotoxin-I inhibiting sodium channel inactivation. AU - Xiao,Yucheng, AU - Li,Jiang, AU - Deng,Meichun, AU - Dai,Changliang, AU - Liang,Songping, Y1 - 2007/05/03/ PY - 2007/02/11/received PY - 2007/04/15/revised PY - 2007/04/23/accepted PY - 2007/7/10/pubmed PY - 2007/11/10/medline PY - 2007/7/10/entrez SP - 507 EP - 17 JF - Toxicon : official journal of the International Society on Toxinology JO - Toxicon VL - 50 IS - 4 N2 - 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. SN - 0041-0101 UR - https://www.unboundmedicine.com/medline/citation/17618665/Characterization_of_the_excitatory_mechanism_induced_by_Jingzhaotoxin_I_inhibiting_sodium_channel_inactivation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041-0101(07)00163-8 DB - PRIME DP - Unbound Medicine ER -