Session: 05-01-02: Injury and Damage Biomechanics: Brain Response at the Cellular Level

Paper Number: 100165

100165 - Effect of Mechanical Stretch on the Action Potential Signal Conduction in Neuronal Axons 

Neurons are prone to deformations as a result of the shear effect between the grey and white matters caused by the rapid and sudden movement of the brain tissue during an event of a mechanical impact or neurodegenerative diseases. These structural damages are significantly prominent in the causation of diffuse axonal injury which comes in the form of stretching primarily and consequently followed by local swelling as a secondary effect. The microstructural alterations, which are brought about as a result of these physical distortions, have a significant impact on the electrophysiological performance of the neuron cells. Earlier research works suggest that the functionality of the axons can be altered by the stretching effect, which may result in a sudden shift in behavior of the action potential (AP) signals. In our study, we aim to investigate the characteristics of the AP signals in a stretch-induced axon through computational models developed to imitate the electrical activity in the neuron cells. We hypothesize that the neuron maintains its signal conduction capabilities up to a certain threshold even after being subjected to mechanical trauma. These postulations are backed up by the findings from several experimentations cited in the preceding literatures. In our model, the axon is represented by a long one-dimensional geometry which has been loaded with mechanical strains of fluctuating magnitudes. The effects of the applied strains on the AP signal transmission across the axon are measured for varying axon radii as well. It is proposed that the strain on the neuron cells instigates the cell membrane to unfold its internal structure in a countermeasure to account for the elongation. Despite this implication, the influence of axonal stretching on the ion channel densities along the membrane is yet to be looked upon further. Apparently, it has been established that the APs spike frequently in a stretched axon with increased conduction speed. Since the membrane electrical parameters are proportional to the axon radius, thicker axons are likely to fire APs faster than thinner axons. In addition, the myelin sheath plays a vital role in the saltatory conduction in axons as well, which necessitates the analysis of the electrical activities in both unmyelinated and myelinated axons simultaneously. In conclusion, the numerical simulations generated with the model assist us to forecast the damage threshold for a neuron cell by analyzing the extent of axonal electrophysiological deficits in response to the injury sustained at the cellular level.

Presenting Author: Md Navid Imtiaz Rifat University of Texas at Arlington

Presenting Author Biography: Mr. Md Navid Imtiaz Rifat is a Graduate Research Assistant in the Department of Mechanical and Aerospace Engineering at the University of Texas at Arlington. His research is related to traumatic brain injury mechanisms to evaluate damage threshold at the cellular level.

Authors:

Md Navid Imtiaz Rifat University of Texas at Arlington
Arthur Koster University of Texas at Arlington
Ashfaq Adnan University of Texas at Arlington