Table 1.
Changes in AP waveform properties across the course of recording
ΔVm (mV) | ΔVthreshold (mV) | ΔAP half-width (% baseline) | ΔAP peak (mV) | Δ rheobase (pA) | n | Baseline EPSP (mV) | Postdrug EPSP (mV) | |
---|---|---|---|---|---|---|---|---|
Time-locked control (15 min) | 0.48 ± 1.05 | −1.34 ± 1.86 | 98 ± 10 | −3.23 ± 5.43 | −10 ± 29.21 | 35 | 5.9 ± 4.6 | 4.6 ± 3.8 |
Conotoxin MVIIC | 0.47 ± 0.54 | −2.12 ± 1.55 | 99 ± 8 | −3.12 ± 2.97 | −21.43 ± 26.73 | 8 | 4.8 ± 3.8 | 0.5 ± 0.4* |
SNX-482 | −0.18 ± 0.72 | −0.92 ± 1.00 | 102 ± 11 | −3.39 ± 5.00 | −14.29 ± 19.67 | 8 | — | — |
TTA-P2 | 0.37 ± 0.65 | −0.90 ± 0.88 | 100 ± 8 | −3.02 ± 2.75 | 7.50 ± 37.36 | 11 | — | — |
Nifedipine | 0.89 ± 0.42 | −0.62 ± 1.42 | 102 ± 5 | −3.12 ± 3.00 | −8.33 ± 25.82 | 5 | — | — |
Conotoxin GVIA | 0.14 ± 0.90 | −0.78 ± 1.46 | 103 ± 5 | −2.64 ± 1.17 | −20.00 ± 20.92 | 5 | 5.3 ± 6.0 | 4.8 ± 5.5 |
Agatoxin TK | 0.55 ± 0.42 | −2.55 ± 0.84 | 104 ± 8 | −2.70 ± 1.71 | −12.50 ± 13.69 | 6 | 5.6 ± 4.1 | 1.5 ± 1.4* |
Ryanodine | 1.49 ± 4.24 | −1.14 ± 1.60 | 106 ± 11 | −5.38 ± 5.62 | −13.46 ± 24.19 | 14 | — | — |
Nickel(II) chloride | −0.26 ± 3.09 | −0.51 ± 2.34 | 102 ± 5 | −2.54 ± 2.58 | −33.33 ± 43.78 | 6 | — | — |
Time-locked control (25 min) | 0.54 ± 0.87 | −3.25 ± 2.37 | 101 ± 7 | −5.16 ± 3.71 | −37.50 ± 37.91 | 6 | 3.7 ± 2.4 | 2.1 ± 0.8 |
CaV antagonist cocktail | 0.37 ± 0.83 | −3.26 ± 2.96 | 105 ± 4 | −2.58 ± 6.08 | −45.00 ± 32.60 | 5 | 2.5 ± 1.5 | 0.5 ± 0.4* |
S1 time-lock control | 0.46 ± 0.96 | −3.09 ± 2.07 | 96 ± 4 | −2.57 ± 1.68 | −8.33 ± 14.43 | 3 | 7.8 ± 2.5 | 7.2 ± 2.8 |
S1 conotoxin MVIIC | 0.58 ± 2.57 | −1.04 ± 1.84 | 98 ± 7 | −6.09 ± 5.48 | 0 ± 86.60 | 3 | 6.0 ± 3.0 | 0.7 ± 0.4* |
*p < 0.05. One-way ANOVAs or two-tailed t tests were performed for each waveform property, as appropriate. Paired t tests were performed for EPSP amplitudes.