Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Action Potential01:14

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
Action Potential01:14

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Analgesic Modulation of Neuroendocrine and Region-Specific Neuropathological Responses Following Blast-Induced Traumatic Brain Injury in Rats.

Journal of neurotrauma·2026
Same author

Pathophysiology-guided biomarkers and therapeutics for precision trauma medicine in polytrauma with musculoskeletal injuries.

Military Medical Research·2026
Same author

The effect of dietary omega-6 fatty acid enrichment in rodent models of military-relevant acute traumatic psychological stress and traumatic brain injury.

Frontiers in microbiomes·2026
Same author

Evaluation of Azithromycin-Bicarbonate against Multidrug-Resistant Pathogens in Topical Murine Models of Infection.

ACS infectious diseases·2025
Same author

A Ferret Model of Blast-Induced Traumatic Brain Injury with Biochemical and Neurobehavioral Outcome Measures.

Journal of neurotrauma·2025
Same author

Blast Overpressure-Induced Neuroinflammation and Axonal Injury in the Spinal Cord of Ferrets.

Brain sciences·2025

Related Experiment Video

Updated: May 24, 2026

Modeling Highly Repetitive Low-level Blast Exposure in Mice
06:00

Modeling Highly Repetitive Low-level Blast Exposure in Mice

Published on: May 24, 2024

Transient changes in neuronal cell membrane permeability after blast exposure.

Peethambaran Arun1, Rania Abu-Taleb, Manojkumar Valiyaveettil

  • 1Blast-Induced Neurotrauma Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA.

Neuroreport
|March 20, 2012
PubMed
Summary

Explosive blast exposure compromises neuronal cell membrane integrity, causing bidirectional molecular transport. This disruption offers a potential mechanism for blast-induced traumatic brain injury (TBI).

More Related Videos

Evaluation of Blood-Brain Barrier Breakdown in a Mouse Model of Mild Traumatic Brain Injury
05:19

Evaluation of Blood-Brain Barrier Breakdown in a Mouse Model of Mild Traumatic Brain Injury

Published on: October 18, 2024

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents
06:09

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents

Published on: November 6, 2020

Related Experiment Videos

Last Updated: May 24, 2026

Modeling Highly Repetitive Low-level Blast Exposure in Mice
06:00

Modeling Highly Repetitive Low-level Blast Exposure in Mice

Published on: May 24, 2024

Evaluation of Blood-Brain Barrier Breakdown in a Mouse Model of Mild Traumatic Brain Injury
05:19

Evaluation of Blood-Brain Barrier Breakdown in a Mouse Model of Mild Traumatic Brain Injury

Published on: October 18, 2024

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents
06:09

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents

Published on: November 6, 2020

Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • The precise biochemical mechanisms underlying explosive blast-induced traumatic brain injury (TBI) and associated long-term neurobehavioral issues remain incompletely elucidated.
  • Understanding these mechanisms is crucial for developing effective TBI treatments and preventative strategies.

Purpose of the Study:

  • To investigate the biochemical mechanisms of blast-induced TBI using an in-vitro shock tube model.
  • To determine the effects of blast exposure on neuronal cell membrane integrity and molecular transport.

Main Methods:

  • Utilized an in-vitro model system employing a shock tube for primary blast exposure.
  • Assessed neurobiological changes in response to varying overpressure doses and exposure times.
  • Measured lactate dehydrogenase release, calcein AM dye release, and TO-PRO-3 iodide uptake in SH-SY5Y human neuroblastoma cells to evaluate cell membrane and nuclear membrane integrity.

Main Results:

  • Blast exposure induced dose- and time-dependent neurobiological changes.
  • Significant release of lactate dehydrogenase into the extracellular medium occurred without cell death, indicating compromised cell membrane integrity.
  • Blast exposure led to an overpressure-dependent increase in bidirectional molecular transport across the neuronal cell membrane and affected nuclear membrane integrity.

Conclusions:

  • Blast exposure significantly perturbs neuronal cell membrane integrity.
  • Increased bidirectional molecular transport across compromised membranes is a potential key mechanism contributing to blast-induced TBI.
  • The in-vitro model system provides valuable insights into the cellular-level effects of blast trauma.