Neurosci Lett 2003 May 15;342(1-2):33-36
Freire-Garabal M, Nunez MJ, Balboa J, Garcia-Vallejo LA, Argibay S, Rodrigo E, Rey-Mendez M.
Neuroimmunology Laboratory, Department of Pharmacology, School of Medicine, C/ San Francisco, s/n. 15782 Santiago de Compostela, A Coruna, Spain
Experimental allergic encephalomyelitis (EAE) is a T-cell inflammatory disease of the central nervous system (CNS) widely considered as an animal model of multiple sclerosis.
In Lewis rats, myelin basic protein-complete Freund's adjuvant (MBP-CFA)-induced EAE is an acute monophasic disease from which animals recover fully.
In our experiments, daily treatment (since day 1 after MBP-CFA inoculation) with the 5-hydroxytryptamine((1A)) (5-HT(1A)) receptor agonist (R)-(+)-8-hydroxy-2-(Dipropylamino)-tetralin (R(+)-8-OH-DPAT) resulted in a dose-related enhancement of neurological and histological signs in EAE-induced rats.
This effect of R(+)-8-OH-DPAT was reduced by the co-administration of the 5-HT(1A) receptor antagonist (N-[2-(4-[2-mehoxyphenil]-1-piperazinyl)-ethyl]-N-2-pyridinylcyclohexanecarboxamide (WAY100635) at the peak of the acute disease.
Moreover, treatment with WAY100635 since inoculation resulted in a delayed onset of the first clinical signs, milder disease and earlier regression of neurological signs along with a decrease in inflammation in the CNS.