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. Author manuscript; available in PMC: 2009 Nov 26.
Published in final edited form as: Neuron. 2008 Nov 26;60(4):657–671. doi: 10.1016/j.neuron.2008.08.029

Figure 8.

Figure 8

LTP in Kv4.2-/- neurons is dependent on NR2B-containing receptors. (A) EPSCs recorded at +40 mV to pharmacologically isolate NR2 subunit fractions. The recording procedure is as in Figure 1D. Each trace was averaged with 30 sweeps. Scale bars: 20 pA, 20 ms. (B) The averaged decay rate of EPSCs shown in (A). (C) The averaged NMDA/AMPA ratio measured with total current charge. (D) Ifenprodil sensitivity of NMDAR EPSCs recorded at -60 mV in Mg2+-free external solution containing DNQX (10 μM). Scale bars: 20 pA, 20 ms. (E) EPSC potentiation induced by 4 Hz stimulation paired with depolarization of 0 mV for 1 min. LTP was induced at the 0 min time point. Scale bars: 20 pA, 20 ms. (F) The effect of ifenprodil on synaptic LTP induction in WT and Kv4.2-/- recordings. Ifenprodil completely blocked the induction of LTP in Kv4.2-/- but not in WT recordings. Although these data most likely indicate that Kv4.2-/-, in ifenprodil, lack sufficient NMDAR activation and associated Ca2+- influx, the present data cannot rule out increased reliance on other ifenprodil-sensitive currents in Kv4.2-/- mice. Scale bars: 20 pA, 20 ms. Error bars represent S.E.M.