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. Author manuscript; available in PMC: 2013 Jun 6.
Published in final edited form as: Mol Cell Neurosci. 2007 Mar 23;35(4):604–624. doi: 10.1016/j.mcn.2007.03.008

Figure 5. Co-expression of DPP10a variant, but not DPP6-S, eliminates the dramatically slowed inactivation associated with KChIP4a.

Figure 5

(A) Families of Kv4.2-mediated current from Xenopus oocytes expressing Kv4.2+KChIP4a. Shown are current traces from −100 mV to +50 mV in 10 mV increments for the first 400 ms. (B) Currents from cells expressing Kv4.2+KChIP4a+DPP10a, elicited by a protocol same as one used in (A). For comparison, normalized current traces at +50 mV were overlapped for Kv4.2+KChIP4a, Kv4.2+KChIP4a+DPP6-S, and Kv4.2+KChIP4a+DPP10a (see inset). Note that DPP10a is able to markedly accelerate inactivation, even in the presence of KChIP4a. (C) Differential effects of DPP6-S (left panel) and DPP10a (right panel) on steady-state inactivation in the presence of KChIP4a. While DPP6-S and DPP10a both produce hyperpolarizing shifts in the steady-state inactivation, the magnitude of shift is greater for DPP10a. Fitting traces represent Boltzmann functions. (C) KChIP4a does not interfere with the ability of DPP10a to accelerate recovery from inactivation. The time course of recovery from inactivation, as fitted by single exponential functions, is identical between Kv4.2+DPP10a and Kv4.2+KChIP4a+DPP10a channels.