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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Neuropharmacology. 2013 Dec 4;79:249–261. doi: 10.1016/j.neuropharm.2013.11.022

Fig. 8.

Fig. 8

Glutamate-induced neuronal injury is reduced in CGCs isolated from AT1A receptor knock-out mice (KO) when compared with wild-type controls (WT). Primary CGCs from wild-type or AT1A knock-out mice were exposed to different doses of glutamate (6.25 to 500 µM). The maximum glutamate-induced LDH release was significantly lower in CGCs obtained from AT1A knock-out mice when compared to those from wild-type mice. Results are Means ± SEM for groups of three independent experiments. ***P < 0.001 vs. WT untreated controls ; #P < 0.05, ###P < 0.001 vs. AT1A KO untreated controls; $P < 0.05, $$$P < 0.001 WT vs. AT1A KO.