Loading…

Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide

Cyclosporine A is the major immunosuppressive agent used for organ transplantation and for the treatment of a variety of autoimmune disorders such as multiple sclerosis. In this work, we investigated the effect of the cyclosporine A on the acetylcholinesterase activity in the cerebral cortex, striat...

Full description

Saved in:
Bibliographic Details
Published in:International journal of developmental neuroscience 2007-06, Vol.25 (4), p.259-264
Main Authors: Mazzanti, Cinthia M., Spanevello, Roselia, Ahmed, Musthaq, Schmatz, Roberta, Mazzanti, Alexandre, Salbego, Fabiano Z., Graça, Dominguita L., Sallis, Eliza S.V., Morsch, Vera M., Schetinger, Maria Rosa C.
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cyclosporine A is the major immunosuppressive agent used for organ transplantation and for the treatment of a variety of autoimmune disorders such as multiple sclerosis. In this work, we investigated the effect of the cyclosporine A on the acetylcholinesterase activity in the cerebral cortex, striatum, hippocampus, hypothalamus, cerebellum and pons of the rats experimentally demyelinated by ethidium bromide. Rats were divided into four groups: I control (injected with saline), II (treated with cyclosporine A), III (injected with 0.1% ethidium bromide) and IV (injected with 0.1% the ethidium bromide and treated with cyclosporine A). The results showed a significant inhibition (p < 0.05) of acetylcholinesterase activity in the groups II, III and IV in all brain structures analyzed. In the striatum, hippocampus, hypothalamus and pons the inhibition was greater (p < 0.005) when ethidium bromide was associated with cyclosporine A. In conclusion, the present investigation demonstrated that cyclosporine A is an inhibitor of acetylcholinesterase activity and this effect is increased after an event of toxic demyelination of the central nervous system.
ISSN:0736-5748
1873-474X
DOI:10.1016/j.ijdevneu.2007.02.005