ABSTRACT
By using electron microscopy, the paranodal region and axo-glial junction were examined in optic nerves of rats aged 14 days. The paranodal region was characterized in longitudinal sections by the sequential termination of the myelin lamellae, beginning proximally with the innermost and ending, at the Ranvier node, with the outermost lamella. The termination of each lamella was accom- panied by a separation of the major dense line of the compact myelin and the consequent formation of a "loop" of glial cytoplasm. Each paranodal loop inde- nted the axonal surface as it became junctionally apposed to the axolemma. The periaxonal extracellular space, 10-20nm in width in the internodal region and reduced at the paranodal junction to approximately 3nm, forming an axo-glial junction, which was thought to be held together by dense structure. The parano- dal junction seems to serve strong adhesion between the apposed axonal and glial membranes. Conduction of the nerve impulses in myelinated axons was saltatory. Axons and sheath cells probably maintain vital communication with one another, presumably at the paranodal junctional complex. This communication was viewed as vital to the stability and maintenance of myelin. We found some clear vesi- cles in axoplasm near the Ranvier node and speculated that there were endocyto- sis and exocytosis in paranodal region. This was a direct morphological evidence supporting metabolic coupling between axons and sheeth cells.
ABSTRACT
Objective To investigate the dynamic expression of nitric oxide synthase(NOS) in the apoptosis of primary cultured rat cortical neruons following hypoxia/reoxygenation(H/R) and the protective role of extract of ginkgo biloba(EGB). Methods The cortical neurons of E16-17 days fetal rat were primarily cultured.The apoptosis model of primary cultured cortical nurons following H/R was established by using W-G staning,electromicroscopy,TUNEL staining.The dynamic expression of NOS different H/R times was investigated with NADPH-diaphorase histochemical method. Results H/R can cause apoptosis of primary cultured rat cortical neurons.In the experiment of H-2R-0,H-4R-0, H-6R-0,H-8R-0 and H-2R 18,H-4R 18,H-6R 18 H-8R 18,the apoptosis cells occurred after 4 hour hypoxia.The increasing of apoptosis cell acted as time-dependence and the peak value was at H-8R 18.The expression of NOS increased both after 2 hour hypoxia and reoxygenation 18 hour after 8 hour hypoxia compared with the normal control group.EGB could inhibit the increasing and decrease the percentage of apoptosis.Conclusion The apoptosis of primary cultured rat cortical neurons could be induced by H/R.The increasing of NO might be one of the mechannisms of apoptosis.EGB could singnificantly inhibit the apoptosis by means of inhibiting the expression of NOS and reducing the production of NO.;