Figure 3.

NMDAR-independent LTP in the hippocampal CA1 region of Ca_v1.2^HCKO mice. fEPSPs in response to stimulation of the Schaffer collaterals were recorded in slices from control (▪) and Ca_v1.2^HCKO (□) mice. a, LTP was induced at time 0 by a 200 Hz tetanic stimulation with the NMDAR antagonist APV (50 μm) present throughout the experiment. The time course of the fEPSP slope represents mean + SEM of experiments in eight slices from five mice for each genotype. Representative fEPSPs recorded at the times indicated (a, b) are shown in the corresponding inset. b, LTP was induced at time 0 by multiple strong 100 Hz tetani with the NMDAR antagonist APV (50 μm) present throughout the experiment. The time course of the fEPSP slope represents the mean + SEM in control (10 slices from 6 mice) and Ca_v1.2^HCKO (14 slices from 6 mice) slices. Representative fEPSPs recorded at the times indicated (a, b) are shown in the corresponding inset. c, LTP_K was induced by superfusing hippocampal slices with aCSF containing 25 mm potassium channel blocker TEA for 15 min (indicated by the bar). The NMDAR antagonist, APV (50 μm), was present throughout the experiment. The time course of the fEPSP slope represents the mean ± SEM in control (15 slices from 12 mice) and Ca_v1.2^HCKO mice (11 slices from 7 mice). Representative fEPSPs recorded at the times indicated (a, b) are shown in the corresponding inset. d, Effect of the protein synthesis inhibitor anisomycin (20 μm) and the MEK1/2 inhibitor U0126 (40 μm) on L-LTP_K in control and Ca_v1.2^HCKO mice. ▪, The magnitude of LTP_K 2 h after treatment with TEA in control mice in normal aCSF, in the presence of anisomycin (n = 8 slices from 5 mice) and U0126 (n = 7 slices from 5 mice) is illustrated. □, The magnitude of LTP_K 2 h after treatment with TEA in control mice in normal aCSF and in the presence of anisomycin (n = 11 slices from 7 mice), respectively, is illustrated. ^*Significant difference (p < 0.05). Calibrations: 20 ms, 1 mV. Error bars indicate SE.