The New Jersey Institute of Technology's
Electronic Theses & Dissertations Project

Title:	Diffuse axonal injury effect on myelinating cells and axons
Author:	Zalk, Jennifer Alison
View Online:	njit-etd2013-008 (x, 65 pages ~ 1.7 MB pdf)
Department:	Department of Biomedical Engineering
Degree:	Master of Science
Program:	Biomedical Engineering
Document Type:	Thesis
Advisory Committee:	Pfister, Bryan J. (Committee co-chair) Kim, Haesun (Committee co-chair) Collins, George (Committee member) Cho, Cheul H. (Committee member)
Date:	2013-01
Keywords:	Diffuse axonal injury Myelin degeneration
Availability:	Unrestricted
Abstract:	There is no supporting evidence whether myelin degeneration in diffuse axonal injury (DAI) of the white matter is due to death of myelinating oligodendrocytes or secondary axotomy. Cortical neurons are not able to remain healthy in culture to have their axons myelinated. Dorsal root ganglion (DRG) neurons have been shown to be myelinated by cortical oligodendrocytes in culture. An in vitro stretch injury model was used to analyze the DRG axon pathology during and after injury. DRG myelinating Schwann cells are analyzed to demonstrate what is expected from injury to oligodendrocytes. DRG axons demonstrated a high tolerance to stretch injury compared to cortical axons, at strains up to 90% without disconnection. Axons showed delayed recovery of the developed distortions from injury to their preinjured orientation. Injured DRG axons developed swellings similar to those found along stretch injured cortical axons and in humans with DAI. The intracellular calcium level showed extracellular entry of calcium during injury and high sustained levels following a severe injury. Undifferentiated Schwann cells showed greater calcium influx from severe injury and the possible release of an extracellular signaling molecule increasing the calcium concentration in uninjured cells. Stretch injured differentiated Schwann cells demonstrated an increase in intracellular calcium at the time of injury and a gradual increase in non-injured cells after injury, possibly induced by extracellular signaling molecules and calcium ions traversing to non- injured cells through gap junctions.