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
Perisynaptic schwann cells 12-13 in rats. Schwann cell precursors then differentiate into Immature Schwann cells from which myelinating and non-myelinating Schwann cells are directly descended. These cells generally appear around embryonic day 13-15 in rats. The differentation of Immature Schwann cells occurs after birth and is dependent on the axons in which the glia are associated. This differentation is known to be reversible, as seen in regeneration models. Perisynaptic Schwann cells develop as non-myelinating Schwann cells and encapsulate the NMJ. PSCs can be attributed to glial lineage by the presence of Calcium binding proteins S100, Glial fibrillary acidic protein (GFAP), and Protein 0.