Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9428886 | Neuroscience Letters | 2005 | 6 Pages |
Abstract
The present study investigated the effects of BmK I, a Na+ channel receptor site 3 modulator purified from the Buthus martensi Karsch (BmK) venom, on the voltage-gated sodium currents in dorsal root ganglion (DRG) neurons. Whole-cell patch-clamping was used to record the tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) components of voltage-gated Na+ currents in small DRG neurons. It was found that the inhibitory effect of BmK I on open-state inactivation of TTX-S Na+ currents was stronger than that of TTX-R Na+ currents. In addition, BmK I exhibited a selective enhancing effect on voltage-dependent activation of TTX-S currents, and an opposite effect on time-dependent activation of TTX-S and TTX-R Na+ currents. The results suggested that the inhibitory effect of BmK I on open-state inactivation might contribute to the increase of peak TTX-S and TTX-R currents, and the enhancing effect of BmK I on time-dependent activation might also contribute to the increase of peak TTX-S currents. It was further suggested that a combined effect of BmK I including inhibiting the inactivation of TTX-S and TTX-R channels, accelerating activation and decreasing the activation threshold of TTX-S channels, might produce a hyperexcitability of small DRG neurons, and thus contribute to the BmK I-induced hyperalgesia.
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Authors
Jin Chen, Zhi-Yong Tan, Rong Zhao, Xing-Hua Feng, Jian Shi, Yong-Hua Ji,