Abstract |
Myelination is a very important procedure of the nervous system. The main purpose of a myelin sheath is to increase the speed at which impulses propagate along the myelinated fiber. Myelin decreases capacitance and increases electrical resistance across the cell membrane. Thus, myelination prevents the electrical current from leaving the axon and helps in the transmission of the electrical signal that is required for the coordination of the vertebrate nervous system between different brain areas. Schwann cells supply the myelin for the peripheral nervous system, whereas oligodendrocytes myelinate the axons of the central nervous system. Loss of myelin in the axons is one of the main reasons for a lot of neurodegenerative diseases.
The cell adhesion molecule TAG-1 is expressed by neurons and glial cells and plays a very important role in axon outgrowth, migration and fasciculation during development. It also plays a very important role in the production and maintenance of myelin. Absence of TAG-1 leads to a lot of abnormalities and axon dysfunctions. One of these is the hypomyelination that occurs in axons.
This hypomyelination may occur either from defects in oligodendrocytes development or from defects during myelination process. In our study we focus in the possible defects during myelination process. The goal of our experiments was to examine if there is any difference in the expression level of specific myelin genes (plp, mbp, cnp, mag, nogo-a) and transcription factors (zfp, mrf) in WT and KO mice for TAG-1 in three different time points: in P10 (initiation of myelination in mice), P21 (pick of myelination in mice) and P30 (end of myelination).
Our results indicate that in TAG-1 KO mice there is an overall delay in the production of myelin genes (plp,mbp, cnp, nogo-a) and probably a delay in myelination. There is also a mechanism that tries to repair this defect through the up-regulation of the transcription factor MRF.
|