Lymphokine mRNA expression in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis is associated with a host recruited CD45R hi/CD4+ population during recovery

1993 ◽  
Vol 48 (1) ◽  
pp. 105-117 ◽  
Author(s):  
Andrew D. Weinberg ◽  
George Wyrick ◽  
Bozena Celnik ◽  
Margarita Vainiene ◽  
Anthony Bakke ◽  
...  
1996 ◽  
Vol 68 (1-2) ◽  
pp. 1-11 ◽  
Author(s):  
Stefan Jung ◽  
Jürgen Zielasek ◽  
Gabriele Köllner ◽  
Torsten Donhauser ◽  
Klaus Toyka ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Grzegorz Sulkowski ◽  
Beata Dąbrowska-Bouta ◽  
Lidia Strużyńska

The aim of our investigation was to characterize the role of group I mGluRs and NMDA receptors in pathomechanisms of experimental autoimmune encephalomyelitis (EAE), the rodent model of MS. We tested the effects of LY 367385 (S-2-methyl-4-carboxyphenylglycine, a competitive antagonist of mGluR1), MPEP (2-methyl-6-(phenylethynyl)-pyridine, an antagonist of mGluR5), and the uncompetitive NMDA receptor antagonists amantadine and memantine on modulation of neurological deficits observed in rats with EAE. The neurological symptoms of EAE started at 10-11 days post-injection (d.p.i.) and peaked after 12-13 d.p.i. The protein levels of mGluRs and NMDA did not increase in early phases of EAE (4 d.p.i.), but starting from 8 d.p.i. to 25 d.p.i., we observed a significant elevation of mGluR1 and mGluR5 protein expression by about 20% and NMDA protein expression by about 10% over the control at 25 d.p.i. The changes in protein levels were accompanied by changes in mRNA expression of group I mGluRs and NMDARs. During the late disease phase (20–25 d.p.i.), the mRNA expression levels reached 300% of control values. In contrast, treatment with individual receptor antagonists resulted in a reduction of mRNA levels relative to untreated animals.


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