Study On Alteration Of Oligodendrocyte In Rats Following Global Cerebral Ischemia

Ischemic stroke is characterized by high morbidity, mortality, mutilation and recurrence. Almost all instances of ischemic stroke involve white matter. The pathophysiology of neuronal death in cerebral ischemia has been intensively studied. In contrast, much less attention has focused on the ischemic damage to glial cells. Oligoden -drocytes are abundant in both gray and white matter of the brain and spinal cord. Oligodendrocytes, myelin-forming cells of the central nervous system, are vulnerable to damage in a variety of neurologic diseases. More importantly, the damage of oligodendro -cytes has profound consequences to the function of myelinated CNS tracts, the white matter. Like neurons, oligodendrocytes are highly sensitive to injury by oxidative stress, excitatory amino acids, trophic factor deprivation and activation of apoptotic pathways. Recently, there is growing awareness that oligodendrocytes are also targets of injury in acute ischemia. In addition, oligodendrocytes are known to be quite vulnerable to ischemic stress, resulting in early loss of myelin after ischemic stress. They appear vulnerable to hypoxia-ischemia in phase specificity. The early oligodendroglial lineage cells may be more susceptible to ischemic injury than the mature oligodendrocyte. Although there are multiple reasons why clinical trails of NMDA receptor antagonists failed to improve outcome in stroke patients, a fundamental biologic issue may relate to their inability to prevent death of oligodendrocytes and damage to axons since neither of which express NMDA receptors. Apparently, any agents that are able to protect the cellular elements of gray and white matter will attenuate neurological function deficit.Partâ… Hemorheology in rats following global cerebral ischemiaObjective To study the hemorheology in rats following global cerebral ischemia. Method The 4-VO procedure was performed on adult male Sprague-Dawley rats,...