Cyclosporine-A treatment prevents apoptosis in rat lumbar ganglion cells

We evaluated the expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 in lumbar ganglion cells of rats by immunohistochemistry under normal conditions and after 7, 14 and 21 days of cyclosporine-A treatment (7 and 15mg/kg/daity). In normal rats, Bax was weakly expressed in all types of neurons, whereas satellite cells showed moderate immunostaining. Bcl-2 expression was weak in type A neurons and weak or moderate in type B and C neurons and also into satellite cells. In cyclosporine-A-treated rats, we found changes in Bax staining of neurons: type A neurons and type B neurons were weakly stained, whereas type C neurons were moderately stained. Bax expression in satellite cells was moderate after 7 days of treatment and increased strongly after 14 and 21 days of treatment. Bcl-2 expression increased significantly in neurons after 14 and even more after 21 days of treatment with 7 mg/kg cyclosporine-A, mainly in type B and C neurons. With 15mg/kg cyclosporine-A, Bcl-2 increased moderately in type A and B neurons and strongly in type C neurons only after 7 days. After 14 and 21 days, Bcl-2 expression was moderate in type A neurons whereas it was strong or even very strong in type B and C neurons. Satellite cells showed a moderate increase in Bcl-2 after 7 and 14 days of treatment whereas after 21 days, expression was strong. We conclude that (1) in normal conditions, Bax and Bcl-2 were differently expressed in neurons and satellite cells; (2) cyclosporine-A treatment rapidly enhanced Bax expression in satellite cells only, whereas Bcl-2 expression increased moderately in type A neurons and was strongly expressed in type B and C neurons; (3) cyclosporine-A has a protective role in neurons but not in satellite cells; and (4) the neuroprotective rote of cyclosporine-A is dose dependent. Furthermore, the strong expression of Bax in satellite cells can explain the temporary nature of the neurotoxic effect commonly observed after cyclosporine-A administration. (C) 2004 Elsevier GmbH. All rights reserved.