摘要
Traumatic injuries to the central nervous system (CNS), in- cluding traumatic brain injury (TBI) and spinal cord injury (SCI), often involve an immediate mechanical damage to plas- ma membrane that surrounds neuronal sornata and axons. This initial disruption of plasma membrane following injuries has been convincingly demonstrated by increased membrane permeability to large molecules and dyes that are normally inaccessible to cellular plasma (Farkas et al., 2006; Cho and Borgens, 2012). Further evidence comes from experiments that showed ultra-structural changes of plasma membranes, axons, and organelles, and subsequent neuronal death and axotomy (Povlishock and Pettus, 1996; Whalen et al., 2008).
Traumatic injuries to the central nervous system (CNS), in- cluding traumatic brain injury (TBI) and spinal cord injury (SCI), often involve an immediate mechanical damage to plas- ma membrane that surrounds neuronal sornata and axons. This initial disruption of plasma membrane following injuries has been convincingly demonstrated by increased membrane permeability to large molecules and dyes that are normally inaccessible to cellular plasma (Farkas et al., 2006; Cho and Borgens, 2012). Further evidence comes from experiments that showed ultra-structural changes of plasma membranes, axons, and organelles, and subsequent neuronal death and axotomy (Povlishock and Pettus, 1996; Whalen et al., 2008).