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. Author manuscript; available in PMC: 2014 Oct 1.
Published in final edited form as: J Neuropathol Exp Neurol. 2013 Oct;72(10):10.1097/NEN.0b013e3182a4b266. doi: 10.1097/NEN.0b013e3182a4b266

Figure 6.

Figure 6

Colocalization analysis for all kainic acid receptor (KAR) subunits at 1 week post-kainic acid (KA)-induced status epilepticus (SE) vs. control. Colocalization areas were measured for each series of optical sections through the tissue slice. Sections (3 per brain) were stained for each KAR subunit and glial fibrillary acidic protein (GFAP), and the results were averaged. Very little to no colocalization was seen in GFAP-positive astrocytes in naïve control tissue (n = 5), and was below the experimentally derived limit of detection (dotted line = mean + 1 SD of colocalization area from combined primary antibody omission slides). For KA-treated tissue samples (n = 6 for each subunit), the GluK1 and GluK4 subunits showed the greatest colocalization followed by modest colocalization of GluK2/3 and GluK5. Data are expressed as mean ± SEM. ns = not significant, *p < 0.05, **p < 0.01, ***p < 0.001.