Fig. 7

TBI alters the axon population excitability without changing the refractory period. A subset of mice had extended studies of additional conduction properties from the ex vivo brain slice preparations as shown in Fig. 6. A The axon intrinsic excitability was probed by measuring the stimulus duration relative to increasing stimulus current. In both N1 and N2 axons, 4-AP treatment shifted the strength-duration curve toward a more excitable state in sham mice, based on eliciting a similar response with a lower stimulus strength at a given stimulus duration. This strength-duration analysis also revealed that TBI induced hyperexcitability of N2 axons in the vehicle condition. The N2 axon hyperexcitability after TBI was similar in the 4-AP and vehicle conditions. B The axon refractory period due to recovery time between action potentials was probed with a paired-pulse protocol. Representative N1 and N2 compound action potential (CAP) waveforms from a single pulse stimulation as compared to a paired-pulse protocol with varying interpulse intervals (IPI). Orange lines from CAP peaks to their projected bases indicate the amplitude of each waveform. Plots of the percent ratio of each second pulse CAP amplitude (CAP₂), evoked in the paired-pulse stimulation, divided by the CAP amplitude of the single reference pulse stimulation (CAP₁) showed no differences in refractoriness between sham and TBI animals or between vehicle and 4-AP treatments. A–B Linear effects model statistical analysis and Holm-Sidak’s multiple comparison test (*p < 0.05, **p < 0.01). Data is expressed as mean ± SEM with n = 6–7 animals per group