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. Author manuscript; available in PMC: 2013 Mar 18.
Published in final edited form as: Seizure. 2011 Feb 10;20(5):395–401. doi: 10.1016/j.seizure.2011.01.010

Fig. 1.

Fig. 1

Calpain was overexpressed in the anterior temporal neocortex of patients with intractable epilepsy. (A) Identification of the expression patterns of μ-calpain in the control and the epileptic human samples by semi-quantitative RT-PCR of mRNA levels. Total RNA was isolated from the anterior temporal neocortex. GAPDH was used as an internal control. Densitometry analysis was performed using FluorChem software. The intensity of bands was quantified and normalized by that of GAPDH. The data are expressed as mean ± SD. The value of *p < 0.05 is indicated as significantly different. (B) Western blot analysis was used to validate the differential displays for inactive μ-calpain and α-spectrin (μ-calpain-mediated breakdown of spectrin) in the control and the epileptic human samples. Total proteins (10 μg/lane) were extracted from human samples by SDS-PAGE for each sample and probed with the primary antibody of μ-calpain. Densitometry analysis was performed using FluorChem software. Representative Western blots qualitatively visualizing μ-calpain expression levels. Histograms of the normalized μ-calpain band intensities for the epileptic group and the control group. The data are expressed as mean ± SD. The value of *p < 0.05 is indicated as significantly different.