Assessment of Membrane Permeability After Traumatic Brain Injury

Traumatic brain and spinal cord injury manifests following structural compromise of the tissue, including neurons and their axons, glial cells, blood vessels and extracellular components, and subsequent secondary injury cascades. The degree of primary injury depends on the cellular orientation within the tissue, local tissue mechanical properties, strain experienced at the cell level, and rate at which the insult is delivered. The plasma membrane may be directly stretched to a point of failure in either a permanent (lethal) or transient (initially sublethal) manner. The acute evidence of membrane damage is a nonspecific increase in membrane permeability immediately following a traumatic insult. Increased membrane permeability has been observed in several in vitro and in vivo models of traumatic neural injury; therefore, understanding the events that occur in the acute and subacute time periods may provide a preclinical basis for protective and/or reparative therapeutic targets. The implementation of a strategy to repair damaged membranes in the injured nervous system, however, requires continued study of the temporal and spatial extents of membrane damage, biomolecules that are acutely damaged, role of ongoing membrane damage due to free radical attacks and other degradative processes, and potential for endogenous repair. Experimental procedures to detect the presence and mechanisms of plasma membrane damage and repair, therefore, should be established in order to scrutinize the link between primary insult parameters and membrane damage and the balance between secondary membrane damage and endogenous repair attempts. The use of various markers to label cells with compromised membranes in TBI models is described, as well as limitations and considerations for future studies.