Article Figures & Data
Figures
- Figure 1.
Pilocarpine-induced SE (pilo-SE) increases the risk of sudden death. Pilocarpine-treated mice (Pilo-SE; n = 15) have a decreased survival rate (23%) compared to control mice (n = 10, 100%; Log-rank Mantel–Cox; p = 0.0002). Mice that survived SE died suddenly and unexpectedly at post-SE time points associated with the development of spontaneous seizures.
- Figure 2.
Increased action potential frequency in GABAergic NTS neurons from pilo-SE mice is dependent on glutamate receptor activation. A, Representative traces showing action potential firing (Na+ currents) in GABAergic NTS neurons in slices from control mice recorded in normal ACSF (nACSF) at three different time points (i.e., 1, 6, and 12 wks) after vehicle treatment. B, Representative traces showing action potential firing in GABAergic NTS neurons from mice that survived pilo-SE under normal recording conditions (nACSF) at three different time points after SE. C, Representative traces of action potential firing in control mice in the presence of kynurenic acid (KYN; 1 mM) at the same time points. D, Representative traces of action potential firing in the presence of KYN in pilo-SE mice. E, Action potential firing frequency is significantly greater in pilo-SE mice compared with age-matched control mice at 1, 6, and 12 wks posttreatment (unpaired t test; *, p < 0.05). F, In the presence of KYN, action potential firing frequency in NTS GABA neurons from pilo-SE mice was not significantly different from that of control mice (unpaired t test; p > 0.05).
- Figure 3.
Significantly increased sEPSC frequency in GABAergic NTS neurons from pilo-SE mice. A, Representative traces showing sEPSCs in a GABAergic NTS neuron from control mice 1, 6, and 12 wks posttreatment. B, Representative traces showing sEPSCs in a GABAergic NTS neuron from pilo-SE mice 1, 6, and 12 wks posttreatment. C, sEPSC frequency is significantly higher in GABAergic NTS neurons from pilo-SE mice compared with control mice 1, 6, and 12 wks posttreatment (unpaired t test; *, significant). D, sEPSC amplitude is not significantly different (unpaired t test; p > 0.05) between control and pilo-SE mice at any time point.
- Figure 4.
Significantly increased mEPSC frequency in GABAergic NTS neurons from pilo-SE mice. A, Representative traces showing mEPSCs in a GABAergic NTS neuron from a control mouse 1, 6, and 12 wks posttreatment. B, Representative traces showing mEPSCs in a GABAergic NTS neuron from a pilo-SE mouse 1, 6, and 12 wks posttreatment. C, mEPSC frequency is significantly higher in GABAergic NTS neurons from pilo-SE mice compared with control mice at 6 and 12 wks posttreatment (unpaired t test; *, p < 0.05). D, mEPSC amplitude is not significantly different between control and pilo-SE mice at any time point (unpaired t test).
- Figure 5.
PPr and frequency-dependent depression are unaltered in pilo-SE mice. A, Representative traces of eEPSC responses in GABAergic NTS neurons 1 wk posttreatment from control and pilo-SE mice. B, Representative traces of eEPSC responses in GABAergic NTS neurons 6 wks posttreatment from control and pilo-SE mice. C, Representative traces of eEPSC responses in GABAergic NTS neurons 12 wks posttreatment from control and pilo-SE mice. D, The PPr was not significantly different between control and pilo-SE mice at any time point posttreatment (unpaired t test; p > 0.05). E, The ratio of the 5th response amplitude to that of the 1st response was also not significantly altered in pilo-SE mice at any time point (unpaired t test; p > 0.05).
Tables
Outcome measure Data structure Type of test Confidence interval a. Survival curve Nominal data, nonnormal distribution Log-rank (Mantel–Cox) 0.03526 to 0.3404 b. Action potential firing frequency ACSF Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: 0.83 to 3.23
Week 6: 0.02 to 2.42
Week 12: 0.01 to 4.10c. Action potential firing frequency KYN Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: –2.28 to 4.61
Week 6: –1.52 to 1.24
Week 12: –2.46 to 1.90d. sEPSC frequency Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: 1.01 to 5.74
Week 6: 0.03 to 2.41
Week 12: 0.12 to 2.30e. sEPSC amplitude Week 1:normal distribution
Week 6:normal distribution
Week 12:normal distributionUnpaired t test Week 1: –4.88 to 6.12
Week 6: –3.93 to 3.56
Week 12: –7.66 to 1.72f. mEPSC frequency Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: –0.54 to 1.52
Week 6: 0.65 to 2.74
Week 12: 0.30 to 1.81g. mEPSC amplitude Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: –4.60 to 5.50
Week 6: –4.96 to 0.97
Week 12: –7.66 to 0.69h. PPr Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1:–0.13 to 0.44
Week 6: –0.12 to 0.66
Week 12: –0.10 to 0.21i. Mean A5/A1 Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: –0.24 to 0.27
Week 6: –0.17 to 0.64
Week 12:–0.09 to 0.29j. Input resistance Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: –2.00 to 1.86
Week 6: –1.12 to 0.75
Week 12: –2.13 to 0.99k. Resting membrane potential Week 1: normal distribution
Week 6: normal distribution
Week 12: normal distributionUnpaired t test Week 1: –18.72 to 8.75
Week 6: –11.82 to 9.65
Week 12:–11.37 to 7.67l. Heart rate Normal distribution Two-way ANOVA Baseline: –73.56 to 100.80
24 h: –188.60 to –14.23
Week 6: –94.12 to 80.28
Week 12: –86.80 to 99.64m. SDNN Normal distribution Two-way ANOVA Baseline: –0.96 to 0.62
24 h: 0.03 to 1.62
Week 6: –0.78 to 0.79
Week 12:n. RMSSD Normal distribution Two-way ANOVA Baseline: –2.63 to 2.11
24 h: –1.87 to 2.97
Week 6: –2.482 to 2.261
Week 12: –0.92 to 0.77- Table 2.
Resting membrane potential and input resistance of GABAergic NTS neurons in mice that survived SE is not significantly different from age-matched control mice at any time point (unpaired t test; p > 0.05)
Time Input resistance (MΩ) Resting membrane potential (mV) Control Pilo-SE Control Pilo-SE Week 1 1160 ± 600 1590 ± 490 –47.65 ± 5.35 –51.69 ± 4.25 Week 6 1369 ± 346 1180 ± 293 –52.23 ± 3.69 –53.32 ± 3.63 Week 12 2477 ± 611 1905 ± 429 –55.93 ± 3.31 –57.57 ± 3.33 Time Control (n = 6) Pilo-SE (n = 8) Heart rate (bpm) SDNN (ms) RMSSD (ms) Heart rate (bpm) SDNN (ms) RMSSD (ms) Baseline 539.42 ±
14.2310.60 ± 0.13 2.96 ± 0.65 525.8 ±
22.0210.77 ± 0.21 3.22 ± 0.38 24 h 534.66 ±
8.9210.68 ± 0.08 3.37 ± 0.51 636.10 ± 39.12 9.85 ±
0.342.86 ± 0.59 Week 6 549.96 ±
12.9310.48 ± 0.13 3.21 ± 1.25 556.90 ± 26.26 10.47 ± 0.23 3.32 ± 0.45 Week 12 530.54 ±
9.2810.68 ± 0.09 3.12 ± 0.66 524.10 ± 18.19 10.75 ± 0.19 3.27 ± 0.62 Heart rate and the standard deviation of the N-to-N interval (SDNN) were increased 24 h after SE, but no differences were detected at other time points (heart rate: two-way ANOVA, F(3,46) = 2.52, p = 0.069; SDNN: two-way ANOVA, F(3,46) = 2.25, p = 0.094). The root mean squared of the standard deviation (RMSSD) was not significantly different at any time point (two-way ANOVA, F(3,46) = 0.135, p = 0.939).
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