Modulation of Neurological Deficits and Expression of Glutamate Receptors during Experimental Autoimmune Encephalomyelitis after Treatment with Selected Antagonists of Glutamate Receptors
Figure 3
Expression of mGluR1 mRNA (a, c, e, and g) and protein (b, d, f, and h) in forebrain of control and EAE rats at different times post-immunization (a and b) and after therapeutic treatment with antagonists of glutamate receptors: amantadine (c and d), memantine (e and f), and LY 367385 (g and h). Total RNA was prepared from healthy control rats, rats with EAE, and rats with EAE after therapy at the indicated d.p.i. The mGluR1 mRNA levels were determined by quantitative real-time PCR (see Section 2) and normalized against actin. Graphs (a), (c), (e), and (g) present the results expressed as percentage of control from four independent experiments. ; ; different versus control (healthy untreated rats). ; ; different versus EAE rats not subjected to therapy in corresponding d.p.i. (one-way ANOVA followed by Dunnett’s multiple comparison posttest). Representative immunoblots show the expression of mGluR 1 receptor protein in forebrain homogenates of (b) control rats and rats with EAE at different times post-immunization, (d) amantadine-treated EAE rats, (f) memantine-treated rats with EAE, and (h) LY 367385-treated rats with EAE. The results are expressed as percentage of control. Graphs (b), (d), (f), and (h) present the results of densitometric analysis, normalized to β-actin, of four independent immunoblots, each done from distinct brain; (one-way ANOVA with post hoc Dunnett’s test).
