Skip to main content
. Author manuscript; available in PMC: 2017 Jul 6.
Published in final edited form as: Mol Pharm. 2017 Mar 2;14(4):999–1011. doi: 10.1021/acs.molpharmaceut.6b00770

Figure 2.

Figure 2

Status epilepticus (high dose SE model) upregulates P-glycoprotein in brain capillaries in vivo. (A) High dose pilocarpine protocol to induce status epilepticus. (B) Western blot showing that P-gp protein expression levels are increased in brain capillary membranes of animals that received one high dose of pilocarpine to induce status epilepticus (SE) compared to control animals that did not receive pilocarpine. P-gp protein expression levels are also slightly increased in brain capillary membranes from rats that received pilocarpine but did not develop SE. This increase is likely due to the few seizures these animals experienced (not a full SE), suggesting a “dose response-like” relation between seizures (glutamate release) and P-gp protein expression levels. β-Actin was used as protein loading control. (C) P-gp transport activity determined as NBD-CSA fluorescence accumulation in brain capillary lumens is increased in capillaries from rats that developed SE. Data are mean ± SEM (n =10–15 capillaries per treatment group; pooled tissue from all rats per group; control group n = 6 rats, pilocarpine group n = 8 rats, status epilepticus group n = 3 rats). Units are arbitrary fluorescence units (scale, 0–255). Statistical comparison (one-way ANOVA): ***, significantly higher than controls, p < 0.001.