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 reduce astrogliosis), and increase GAP-43 expression, a useful protein marker for neurite growth. Moreover, reduced astrocyte proliferation decreases expression of chondroitin sulfate proteoglycans (CSPGs), major extracellular matrix molecules associated with inhibition of neuroregneration after trauma to the CNS. Recent work has also shown that olomoucine suppresses microglial proliferation within the glial scar. This is particularly important because microglia play an important role in the secondary damage following lesion to the CNS, during the time of scar formation. Microglial cells are activated via various pro-inflammatory cytokines (some discussed above). Rat spinal cord injury models have shown remarkable improvements after the administration