Previous studies revealed that during development the laminin immunopositivity gradually disappeared from the brain vessels, but temporarily re-appeared in them around lesions. The question of the present study was the correlation between the post-lesional vascular immunopositivity to laminin and the glial reaction. Following stab wounds, double fluorescent immunohistochemical labelling was performed against laminin (using a polyclonal antiserum against laminin 1) and glial fibrillary acidic protein. A number of vessels exhibited intense immunopositivity to laminin within the lesioned tissue. Where these laminin immunopositive vessels entered the perilesional brain substance, the astroglia formed contacts on them, and the separate vascular and glial basal laminae fused. The disappearance of the post-lesional laminin immunopositivity seemed to coincide with these phenomena. When monoclonal antibodies were applied against the beta1 and gamma1 laminin chains, vessels proved to be immunopositive at the lesion, but none in the intact brain tissue. No immunoreactivity was detected in the cases of alpha2 and beta2 chains. The results suggest that the disappearance of laminin immunopositivity may be attributed to that the epitopes become inaccessible for antibodies owing to the formation of gliovascular junctions and common basal lamina between astroglia and vessel. The possible role of an alteration in the laminin composition and the effect of fixation are discussed.

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 beta-dystroglycan, glial fibrillary acidic protein (GFAP), and laminin following stab wounds in adult rats. In intact brain the vessels were immunopositive to beta-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 beta-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 beta-dystroglycan. When glial reaction regressed, the beta-dystroglycan immunopositivity re-appeared, and laminin immunopositivity became undetectable again. Post-lesional disappearance of vascular beta-dystroglycan immunostaining was described earlier, and was attributed to the cleavage of beta-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 beta-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 beta-dystroglycan, glial reaction and detectability of laminin. Manifestation of laminin immunoreactivity also indicates gliovascular decoupling. Coincidence between glial reaction and lack of vascular beta-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.

No abstract

Estrogen is one of the most important female sex hormones, and is indispensable for reproduction. However, its role is much wider. Among others, due to its neuroprotective effects, estrogen protects the brain against dementia and complications of traumatic injury. Previously, it was used mainly as a therapeutic option for influencing the menstrual cycle and treating menopausal symptoms. Unfortunately, hormone replacement therapy might be associated with detrimental side effects, such as increased risk of stroke and breast cancer, raising concerns about its safety. Thus, tissue-selective and non-classical estrogen analogues have become the focus of interest. Here, we review the current knowledge about estrogen effects in a broader sense, and the possibility of using selective estrogen-receptor modulators (SERMs), selective estrogen-receptor downregulators (SERDs), phytoestrogens, and activators of non-genomic estrogen-like signaling (ANGELS) molecules as treatment.