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
Guidepost cells set of guidepost cells present for TCA guidance. These GABAergic neurons migrate to the medial ganaglionic eminence (MGE) region to form a "corridor" between proliferation zones of the MGE and globus pallidus (GP). Corridor cells provide TCA growth through MGE-derived regions. However, the Neurgulin1 signaling pathway needs to be activated, with the expression of ErbB4 receptors on the surface of TCAs, for the connection to occur between corridor cells and TCAs. There are subpopulations of glial cells that provide guidance cues for axonal growth. The first set of cells, called the "mid-line glial zipper", regulate the midline fusion and guidance