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 fibrillary acidic protein a type III IF protein that maps, in humans, to 17q21. It is closely related to its non-epithelial family members, vimentin, desmin, and peripherin, which are all involved in the structure and function of the cell’s cytoskeleton. GFAP is thought to help to maintain astrocyte mechanical strength, as well as the shape of cells but its exact function remains poorly understood, despite the number of studies using it as a cell marker. Glial fibrillary acidic protein (GFAP) was named and first isolated and characterized by Lawrence F. Eng in 1969. Type III intermediate filaments contain three domains, named the head,