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Following brain lesions, the gliovascular basal lamina undergoes destruction and the gliovascular connections ‘decouple’. Laminin receptors, as dystroglycan, are essential in these processes. The present study compares the immunoreactivities of β-dystroglycan, glial fibrillary acidic protein (GFAP), and laminin following stab wounds in adult rats. In intact brain the vessels were immunopositive to β-dystroglycan, whereas the laminin of their basal lamina proved to be unavailable to immunoreactions. Following stab wound, however, the adjacent vessels lost their immunopositvity to β-dystroglycan, whereas immunopositivity to laminin became detectable in them. In an advanced stage of glial reaction the territory of GFAP immunopositive reactive astrocytes coincided with the area where vessels lost their immunopositivity to β-dystroglycan. When glial reaction regressed, the β-dystroglycan immunopositivity re-appeared, and laminin immunopositivity became undetectable again. Post-lesional disappearance of vascular β-dystroglycan immunostaining was described earlier, and was attributed to the cleavage of β-dystroglycan by matrix metalloproteinases as a mechanism of the decoupling of the gliovascular connections. Our results, which were obtained in a different type of lesion support that the loss of vascular β-dystroglycan immunopositivity is a general phenomenon following cerebral lesions, and an indirect marker of gliovascular decoupling. For the first time coincidences were presented between vascular immunonegativity to β-dystroglycan, glial reaction and detectability of laminin. Manifestation of laminin immunoreactivity also indicates gliovascular decoupling. Coincidence between glial reaction and lack of vascular β-dystroglycan suggests mutual enhancement between them. The observations may have clinico-pathologic importance since similar investigations may help to follow the progression and regression of post-lesion processes.

Following brain lesions, the gliovascular basal lamina undergoes destruction and the gliovascular connections ‘decouple’. Laminin receptors, as dystroglycan, are essential in these processes. The present study compares the immunoreactivities of -dystroglycan, glial fibrillary acidic protein (GFAP), and laminin following stab wounds in adult rats. In intact brain the vessels were immunopositive to -dystroglycan, whereas the laminin of their basal lamina proved to be unavailable to immunoreactions. Following stab wound, however, the adjacent vessels lost their immunopositvity to -dystroglycan, whereas immunopositivity to laminin became detectable in them. In an advanced stage of glial reaction the territory of GFAP immunopositive reactive astrocytes coincided with the area where vessels lost their immunopositivity to -dystroglycan. When glial reaction regressed, the -dystroglycan immunopositivity re-appeared, and laminin immunopositivity became undetectable again. Post-lesional disappearance of vascular -dystroglycan immunostaining was described earlier, and was attributed to the cleavage of -dystroglycan by matrix metalloproteinases as a mechanism of the decoupling of the gliovascular connections. Our results, which were obtained in a different type of lesion support that the loss of vascular -dystroglycan immunopositivity is a general phenomenon following cerebral lesions, and an indirect marker of gliovascular decoupling. For the first time coincidences were presented between vascular immunonegativity to -dystroglycan, glial reaction and detectability of laminin. Manifestation of laminin immunoreactivity also indicates gliovascular decoupling. Coincidence between glial reaction and lack of vascular -dystroglycan suggests mutual enhancement between them. The observations may have clinico-pathologic importance since similar investigations may help to follow the progression and regression of post-lesion processes.

In earlier studies we have established that rat cortical synaptosomes isolated after a 2-h postmortem storage period showed functional performance and morphological characteristics similar to those isolated immediately after decapitation. The present paper is an account of further functional studies involving the activity of Na-K- and Mg-dependent ATPase and the binding of ouabain in postmortem synaptosomes. These functions were found to survive without major alteration even in the 6-h postmortem fractions. On the other hand the 6-h postmortem fractions showed a very slow oxygen consumption unaffected by DNP and veratrine. In both control and postmortem synaptosomes the actual activity of Na-K-ATPase as calculated from the ouabain-sensitive component of oxygen consumption was consistently less than the potential activity of the enzyme revealed if determination was carried out on the basis of phosphate splitting.

Histological effects of in utero neutron irradiation (0.5 Gy) were investigated in fetal mouse cerebellum. Irradiation was performed on the 18th embryonic day. Histological alterations were examined at 2, 6 and 12 h after irradiation. The effect was most pronounced in the EGL, 6h after irradiation. In some cells (about 24%) karyopycnosis, destruction of cytoplasmic organelles and shrinkage were observed. Remnants of destroyed cells-the pycnotic nuclei with some cytoplasmic debris around them-were rapidly phagocytized by the surrounding cells. In addition to glial elements, the EGL germinal cells also showed phagocytic activity. Dense particles appearing light-microscopically as pycnotic nuclei, proved to be mostly remnants of destroyed, phagocytized cells under electron microscope.