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EN
Postnatal neovascularization has been previously considered synonymous with angiogenesis but it was found that circulating endothelial progenitor cells may home into sites of neovascularization and their differentiation into endothelial cells is consistent with vasculogenesis. In this study, we investigated neovascularization of the adult rat?s cerebral cortex after surgical brain injury by electron microscopic ultrastructural and immunocytochemical studies. We found places with disrupted brain parenchyma. The blood vessels showed an incomplete endothelial lining. In the brain parenchyma, we observed fibrin likely derived from disrupted blood vessels. In the plasma there were cell aggregates characterized by endothelial-like features with fibrils in the cytoplasm, untypical for endothelial cells. These endothelial-like cells participated in the process of new vessel formation. We used the anti-alphaV beta3 integrin antibody to visualize the different morphogenic stages of newly formed blood vessels. We demonstrated the relationship between alphaV beta3 integrin localization and different stages of new vessel formation. Our data suggest that growth and development of new blood vessels due to neovascularization following trauma of the adult rat brain are not restricted to angiogenesis but encompass vasculogenesis as well.
EN
We investigated the features of newly formed blood vessels after surgical brain injury of the rat?s cerebral cortex distal to the operated region. We document the process of split mature blood vessels by an endothelial bridge and morphological features of newly formed vessels. We did not observe a disruption of brain parenchyma. The endothelial lining in vessels was complete. The morphological features of the endothelial cells and basement membrane show that non-sprouting angiogenesis takes place distally to the surgical injury.
EN
Morphological changes of microvessels of cerebral cortex were evaluated in a model of cerebral infarction initiated by a photochemical reaction. Rats were treated with intravenous injection of rose Bengal and irradiated from a halogen lamp source through an intact cranium to precipitate microvascular damage. Investigations in transmission and scanning electron microscopy revealed platelet aggregation on endothelial cells preceded by its early ultrastructural damage. Other typical microscopic features of brain ischaemic injury were present suggesting that the present method may be used as a model for investigating ischaemic brain damage. Since the photochemical activation of the rose Bengal dye results in formation of reactive oxygen species this model may be particularly useful to elucidate the role of free radical-mediated endothelial damage in the formation of microthrombi and blood-brain-barrier integrity.
EN
Streptozotocin (STZ) is a bacterial toxin which selectively damages both insulin-producing cells and insulin receptors. Injections of STZ into the cerebral ventricles of experimental animals are followed by sustained biochemical, metabolic and behavioral effects resembling those which are found in human brains afflicted by Alzheimer's disease. The aim of the present study was to assess the effects of double intracerebroventricular application of STZ on the ultrastructure of rat frontoparietal cortical neurons. The most prominent change, seen 3 weeks after STZ injection, was a significant enlargement of the Golgi apparatus caused by expansion of the trans-Golgi segment of the cellular protein secretory pathway. Morphometric analysis revealed that the area of the trans part of the Golgi complex in neuronal cells was increased more than two-fold (median values: 312 ? 103 nm3 in 14 neurons from control animals, and 846 ? 103 nm3 in 19 neurons from STZ-treated animals, P=0.0012), whereas that of the cis part did not significantly change. The effects of STZ did not resemble Golgi atrophy and fragmentation described in neurons from disease-prone brain structures of patients with Alzheimer's disease, but were similar to that observed after intravenous application of a non-metabolizable glucose analog 2-deoxyglucose. Considering that proamyloidogenic processing of beta-amyloid precursor protein may occur preferentially in the trans-Golgi segment, the observed early response of neuronal ultrastructure to desensitization of insulin receptors may predispose cells to form beta-amyloid deposits.
EN
The effects of a single intraperitoneal injection of a non-metabolizable glucose analog 2-deoxyglucose (2-DG, 500 mg/kg) on the levels of b-APP expression, and phosphorylated and unphosphorylated tau protein in the rat cerebral cortex were investigated. The effects of 2-DG on the ultrastructure of cortical neurons with particular emphasis on the morphology of the Golgi apparatus, and on brain bioenergetics assessed by in vivo 31P-MRS technique were also evaluated. Seven and a half hours after injection of 2-deoxyglucose a significant increase in brain cortex b-APP expression, increased tau phosphorylation, and a marked relative expansion of the trans- part of the Golgi intracellular secretory pathway in cortical neurons has been found. The changes of b-APP expression and tau phosphorylation appeared within 1 h after 2-DG application and continued for at least 24 h. However, brain 31P resonance spectra remained unchanged for up to 7.5 h after 2-DG. It is suggested that the increase of b-APP expression represents a response of brain tissues to 2-DG-evoked biochemical stress, while tau hyperphosphorylation and the change in Golgi morphology may be secondary phenomena.
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