Overview
- Diochot, S. et al. (1998) J. Biol. Chem. 273, 6744.
- Liu, P. et al. (2012) J. Neurophysiol. 107, 3155.
Alomone Labs BDS-I enhances the current of NaV1.7 channels expressed in Xenopus oocytes.A. Time course of BDS-I (#STB-400) effect on the normalized area of NaV1.7 channel current. Membrane potential was held at -100 mV, current was elicited by a 100 ms voltage step to 0 mV every 1 sec, and was significantly enhanced by 3.5 min application of 100 nM BDS-I, indicated by the horizontal bar. B. Superimposed traces of NaV1.7 current upon application of control and of 100 nM BDS-I (as indicated), taken from the recording shown in A.
BDS-I is a 43 amino acid peptidyl toxin isolated from the sea anemone Anemonia sulcata venom. It is reported to be a selective blocker of KV3.4 K+ channel. BDS-I blocks 60% of the KV3.4 current in COS-transfected cells at a concentration of 2.5 µM. The blocking effect is rapid, direct and reversible1. Recently it was shown that it blocks other KV3 channels with similar potencies2.
BDS-I inhibits KV currents in carotid body cells3, an effect which disappears after chronic hypoxia, establishing the unique role played by KV3 channels in the response to hypoxia4. BDS-I (2.5 µM) also reduces the native transient K+ current and increases the action potential duration in hippocampal granule neurons5. In corneal epithelial cells BDS-I (400 nM) inhibits most of the detected KV current6. In magnocellular neurosecretory neurons of the hypothalamus, 100 nM BDS-I inhibits about half of the KV current and increases the action potential duration7. In fast spiking neurons from different brain areas, 2 µM BDS-I inhibits part of the KV current and broadened the action potential and reduces spike frequency8.
BDS-I also produces broadening of the spike and accelerates the upstroke of the action potential by modulating voltage-gated Na+ channels. It enhances TTX-sensitive Na+ channels (highly effective on NaV1.7 channels), and weakly inhibits TTX-resistant NaV channels9.
