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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 3. In the absence of Kv4.2 N-terminal domain, voltage-dependence of inactivation is also determined by the DPP10 variant present.

Figure 3

The N-terminal domain (residues 2-40) of Kv4.2 was genetically removed to eliminate the endogenous fast inactivation. (A) Outward currents from oocytes expressing ΔN2-40, ΔN2-40 plus DPP10a, ΔN2-40 plus DPP10c, and ΔN2-40 plus DPP10d were measured by depolarizing steps of 1 sec duration. Note that the scale bars for current amplitudes differ, indicating that all DPP10 variants increase the current expression of ΔN2-40 channels. (B) Overlapped 800-ms-long traces at +50 mV for ΔN2-40 with and without DPP10a, DPP10c, and DPP10d. (C) Normalize and overlapped traces at +50 mV for 500 ms. Note that, in both panels B and C, acceleration of inactivation by DPP10a does not require the Kv4.2 N-terminal domain. (D) Half-inactivation time as a function of voltage. The results are similar to those in Fig. 6D. (E) Measurement of channel activation by plotting the peak conductance-voltage relationship. Co-expression of DPP10 variants results in differential leftward shifts in the conductance-voltage relationship (g-V). (F) Voltage-dependence of steady-state inactivation for Kv4.2, ΔN2-40, and ΔN2-40 plus DPP10 variants. Both g-V and SSI were fitted with Boltzmann functions. Note that the relative order of leftward shifts observed in g-V curves (DPP10c > DPP10d > DPP10a) is preserved with the steady-state inactivation curves. (F) Recovery from inactivation associated with DPP10 variants. Fitting traces represent single exponential functions.