Mechanism of anoxic depolarization in the brain disruption. Other consequential damage that occurs includes lipolysis, proteolysis, cell swelling, microtubule disaggregation, and DNA fragmentation. Neurons are more susceptible to brain ischemia than the supporting glial cells, because neurons have higher energy demand, conduct an action potential, and produce glutamate, whereas glial cells lack those properties. Yet neurons differ among themselves in their sensitivity to ischemia, depending on the specific properties they exhibit, relating to their locations in the brain. "Selective vulnerability" is the term used to describe how some parts of the brain are more sensitive to anoxia than others, and thus to ischemic insult. Anoxia-prone cells in
Glial scar animal). Further, a reduction in astrocytes and microglia, as well as a reduction in inflammation and angiogenesis, were observed. Interleukin-6 (IL-6) is thought to be a molecular mediator of glial scar formation. It has been shown to promote differentiation of neural stem cells into astrocytes. A monoclonal antibody, MR16-1, has been used to target and block the IL-6 receptors in rat spinal cord injury models. In a study by Okada "et al.", mice were intraperitoneally injected with a single dose of MR16-1 immediately after generating a spinal cord injury. Blockade of IL-6 receptors decreased the number of astrocytes present at