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Updated: Jul 4, 2025

Stretch in Brain Microvascular Endothelial Cells cEND as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

Stretch in Brain Microvascular Endothelial Cells cEND as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

Published on: October 26, 2013

Stretch-Induced Injury Affects Cortical Neuronal Networks in a Time- and Severity-Dependent Manner.

Dylan Sullivan^1,2, Brandon J Vaglio^1,3, Marina M Cararo-Lopes^1,2

¹Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.

Annals of Biomedical Engineering

|January 31, 2024

Summary

Mechanical injury from traumatic brain injury (TBI) alters neuron network activity over time. Changes in electrophysiological properties depend on injury severity and prior neuron synchronization.

Keywords:

Cortical neurons Neuronal network Primary cultures Stretch-induced injury Stretchable microelectrode array

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Time-dependent Increase in the Network Response to the Stimulation of Neuronal Cell Cultures on Micro-electrode Arrays

Time-dependent Increase in the Network Response to the Stimulation of Neuronal Cell Cultures on Micro-electrode Arrays

Published on: May 29, 2017

Area of Science:

Neuroscience
Biomedical Engineering
Cellular Biology

Background:

Traumatic brain injury (TBI) is a major cause of death and disability worldwide.
TBI leads to cognitive decline and neurodegeneration, with no current treatments for TBI-induced cell damage.
Understanding the cellular mechanisms of TBI-induced cell damage is crucial.

Purpose of the Study:

To model primary TBI injury using stretchable microelectrode arrays (sMEAs).
To investigate the electrophysiological effects of mechanical injury on cortical cells.
To analyze changes in neural network activity following TBI-like physical trauma.

Main Methods:

Utilized stretchable microelectrode arrays (sMEAs) to induce and model primary TBI.
Recorded electrophysiological activity of cortical neuron networks before and after mechanical stretching.
Analyzed changes in spike rate, Fano factor, burstlet properties, synchrony, network efficiency, and Q statistic at 1, 24, and 72 hours post-injury.

Main Results:

Mechanical injury significantly altered the firing properties of cortical neuron networks.
Electrophysiological changes were dependent on the time elapsed since injury and the severity of the mechanical stretch.
The degree of neuronal synchronization prior to injury influenced the observed electrophysiological changes post-injury.

Conclusions:

Mechanical forces in TBI cause time- and severity-dependent changes in cortical neuron network electrophysiology.
Neuronal network synchronization plays a critical role in modulating the response to mechanical injury.
This study provides insights into the cellular mechanisms underlying TBI and highlights the importance of network dynamics.