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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Acute axon damage and demyelination are mitigated by 4-aminopyridine (4-AP) therapy after experimental traumatic brain injury

Fig. 1

Experimental study design and key assessments of group allocation. A Graphical representation of experimental timeline and treatment groups. Three sets of experiments were conducted according to pre-determined study designs. For each study, the strain and number of mice used is shown along with the study endpoint and method of analysis of corpus callosum axons. Excl. = number of mice excluded based on pre-determined criteria (see Materials and Methods for definition). B TBI increased the time to right from supine to prone position immediately after surgery (righting reflex) as compared with respective sham groups. This confirms that mice randomized for allocation to the TBI vehicle and TBI 4-AP groups exhibited similar righting times prior to initiating 4-AP treatment. C 4-AP treatment did not cause a significant change in body weight over the period of the experiment. D 4-AP serum drug level concentrations are within the clinical therapeutic target range (20–100 ng/ml) in cardiac blood collected approximately 30–60 min after last 4-AP injection. Graphs show the mean ± SEM with each mouse as an individual data point. One-way ANOVA with Tukey’s multiple comparisons test: B F3,145 = 211.3, p < 0.0001, C F3,145 = 1.057, p = 0.3692. Two-way ANOVA with Holm-Sidak post hoc test: D Interaction: F1,185 = 0.1281, p = 0.7213; Injury F1,185 = 0.0183, p = 0.8927; Drug; F1,185 = 332.8, p < 0.0001

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