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This Article Full Text Full Text (PDF) All Versions of this Article: 584/3/755    most recent jphysiol.2007.140145v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wang, Z. Articles by Fedida, D. Search for Related Content PubMed PubMed Citation Articles by Wang, Z. Articles by Fedida, D. Related Collections Cellular

¹ Department of Anaesthesiology, Pharmacology and Therapeutics, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, Canada V6T 1Z3
² Neuroscience Research Group, Institute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK

Kv3 channels have a major role in determining neuronal excitability, and are characterized by ultra-rapid kinetics of gating and a high activation threshold. However, the gating currents, which occur as a result of positional changes of the charged elements in the channel structure during activation, are not well understood. Here we report a study of gating currents from wild-type Kv3.2b channels, expressed in human embryonic kidney (HEK) cells to facilitate high time-resolution recording. On-gating currents (I_g,on) had extremely rapid kinetics such that at +80 mV, the time constant for the decay of I_g,on was only 0.3 ms. Decay of I_g,on appeared mono-exponential at all potentials studied, and in support of this, the charge–voltage (Q–V) relationship was fitted with a single Boltzmann function, supporting the idea that only one charge system is required to account for the time course of I_g,on and the voltage dependence of Q_on. The voltage (V) for half movement of gating charge was –8.4 ± 4.0 mV (n = 6), which closely matches the voltage dependence of activation of Kv3.2b ionic currents reported before. Depolarizations to more positive potentials than 0 mV decreased the amplitude and slowed the decay of the off-gating currents (I_g,off), suggesting that a rate-limiting step in opening was present in Kv3 channels as in Shaker and other Kv channels. Return of charge was negatively shifted along the potential axis with a V of Q_off of –80.9 ± 0.8 mV (n = 3), which allowed 90% charge return upon repolarization to –100 mV. BDS-II toxin apparently reduced I_g,on, and greatly slowed the kinetics of I_g,on, while shifting the Q–V relationship in the depolarizing direction. However, the Q–V relationship remained well fitted by a single Boltzmann function. These data provide the first description of Kv3 gating currents and give further insight into the interaction of BDS toxins and Kv3 channels.

(Received 5 July 2007; accepted after revision 11 September 2007; first published online 13 September 2007)
Corresponding author D. Fedida: Department of Anaesthesiology, Pharmacology and Therapeutics, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, Canada V6T 1Z3. Email: fedida{at}interchange.ubc.ca

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