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Third, the hippocampus is one of the brain regions most sensitive to ischemia.Finally, the distinct laminar structure of the hippocampus and its precisely mapped synaptic connections allow exact celltype or layerspecific measurements.The most obvious signs of neurodegeneration are the loss of neuronal cell bodies and synaptic contacts.Cerebral hypoperfusioninduced neuronal cell death can be visualized with conventional dyes such as hematoxylineosin, cresyl violet, or toluidine blue, or with more sophisticated techniques such as the TUNEL labeling of apoptotic neurons. The conventional staining procedures revealed no conspicuous loss of neurons during the first week after VO induction. Later, however, increasing neuronal <a href="http://inhibit07.online/archives/226">reasch Benzyl alcohol</a> damage was noted.At weeks, of the animals exhibited hippocampal injury in the CA subfield. At weeks, this had increased to, while at weeks, total hippocampal destruction was observed in of the VO rats. Thus, both technical approaches demonstrated that the neurodegeneration in the hippocampus gradually progressed with time.The predominant type of neuronal cell death in chronic cerebral hypoperfusion has so far remained an unresolved issue.In ischemic brain injury, both modes of cell death occur, represented in a spatial and temporal distribution determined by the severity of the ischemia. The key determinant for the mode of neuronal death is the intracellular concentration of ATP.As a basic approach, apoptosis takes place in the presence of ATP, while necrosis is typically characterized by lack of the energy substrate. As mentioned above, in the initial phase of VO, ATP is rapidly depleted, but the ATP level returns to the control by weeks after the onset of VO. VO, as also evidenced by the CA pyramidal cell morphology in hematoxylineosin or cresyl violetstained sections, while the delayed neuronal death could be apoptotic. The presented results lead to the question of whether the neuronal damage observed at long survival times after VO initiation is induced by the initial, ischemic phase of cerebral hypoperfusion, or whether it is the outcome of a longlasting neurodegeneration caused by the chronic, oligemic phase of VO.In view of the limitations of the VO model in this respect, this issue is difficult to resolve, but it is probable that both the early ischemic and the later oligemic components contribute to the hippocampal neuron loss   and result in a continuous spectrum of necrotic and apoptotic cell death.Chronic cerebral hypoperfusion also affects the dendritic arborizations and synaptic contacts.Microtubuleassociated protein is a cytoskeletal phosphoprotein associated with dendritic microtubules that is thought to reflect dendritic branching, remodeling, and plasticity and has been regarded as a highly sensitive marker of ischemic brain damage. Both the mRNA and the protein concentration of MAP fell from weeks to weeks after the induction of VO, indicating a B R A I N R E S E A R C H R E V I E W S progressive loss of dendrites.A number of studies have been made of the presence and time course of reactive astrocytosis in chronic cerebral hypoperfusion with the help of GFAP immunocytochemistry.Even though astrocytic proliferation was already detected in the cortex and visual pathways after week of VO, an increased GFAP signal was not discerned in the hippocampus until months later.

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