Modulation of Neurological Deficits and Expression of Glutamate Receptors during Experimental Autoimmune Encephalomyelitis after Treatment with Selected Antagonists of Glutamate Receptors
Figure 5
Expression of mRNA of NMDARs (a, c, and e) and protein (b, d, and f) in forebrain of control and EAE rats at different times post-immunization (a and b) and after therapeutic treatment with antagonists of NMDA receptors: amantadine (c and d) and memantine (e and f). Total RNA was prepared from healthy control rats, rats with EAE, and rats with EAE after therapy at the indicated d.p.i. Levels of NMDA mRNAs were determined by quantitative real-time PCR (see Section 2) and normalized to actin. Graphs (a), (c), and (e) present the results expressed as percentage of control from four independent experiments. versus control (one-way ANOVA followed by Dunnett’s multiple comparison posttest). Representative immunoblots show the expression of NMDA receptor protein in forebrain homogenates of (b) control rats and rats with EAE at different times post-immunization, (d) amantadine-treated rats with EAE, and (f) memantine-treated rats with EAE. The results are expressed as percentage of control. Graphs (b), (d), and (f) present the results of densitometric analysis of four independent immunoblots, normalized to β-actin, each done from distinct brain. (one-way ANOVA with post hoc Dunnett’s test).
