Spinal motoneuron synaptic plasticity during the course of an animal model of multiple sclerosis.

• Grant number: 06/04889-9
• Support Opportunities: Regular Research Grants - Publications - Scientific article
• Start date: November 01, 2006
• End date: April 30, 2007
• Field of knowledge: Biological Sciences - Morphology - Anatomy
• Principal Investigator: Alexandre Leite Rodrigues de Oliveira
• Grantee: Alexandre Leite Rodrigues de Oliveira
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

During the course of experimental autoimmune encephalomyelitis (EAE), a massive loss of motor and sensitive function occurs, which has been classically attributed to the demyelination process. In rats, the clinical signs disappear within five days following complete tetraplegia, indicating that demyelination might not be the only cause for the rapid evolution of the disease. The present work investigated the occurrence of EAE-induced changes of the synaptic covering of spinal motoneurons during exacerbation and after remission. The terminals were typed with transmission electron microscopy, as C-, F- and S-type. Immunohistochemical analysis (IH) of synaptophysin, GFAP and the microglia/macrophage marker F4/80 were also used, in order to draw a correlation between the synaptic changes and the glial reaction. The ultrastructural analysis showed that during exacerbation, there was a strong retraction of both F and S type terminals. In this sense, both the covering as well as the length of the remaining terminals suffered great reductions. However, the retracted terminals rapidly returned to apposition, although the mean length remained shorter. A certain level of sprouting may have occurred, since after remission, the number of F terminals was greater than in the control group. The IH analysis showed that the peak of synaptic loss was coincident with an increased macro and microglial reaction. Our results suggest that the major changes occurring in the spinal cord network during the time course of the disease may give a significant contribution to the origin of the clinical signs as well as help to explain their rapid recovery. (AU)