Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Secondary Spinal Cord Injury llI: Pathophysiology

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...

Mitochondrial Membranes

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...

You might also read

Related Articles

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

Sort by

Same author

Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury.

Acta neuropathologica communications·2026

Same author

Trafficking of protein kinases to mitochondria: Implications for ischemic stroke.

Experimental gerontology·2026

Same author

Spatial, temporal and sex specific mitochondrial dynamic changes in severe controlled cortical impact mouse model of traumatic brain injury.

bioRxiv : the preprint server for biology·2026

Same author

Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury.

bioRxiv : the preprint server for biology·2026

Same author

Glial cytokine modulation improves sleep and circadian disruption in female SAA knock-in mice of Alzheimer's-related pathology.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026

Same author

Dim light at night impacts circadian rhythms and Alzheimer's disease-like neuroinflammation and neuropathology in humanized APP SAA knock-in mice.

Sleep·2026

Search research articles

Related Experiment Video

Updated: Jun 21, 2026

A Novel and Translational Rat Model of Concussion Combining Force and Rotation with In Vivo Cerebral Microdialysis

A Novel and Translational Rat Model of Concussion Combining Force and Rotation with In Vivo Cerebral Microdialysis

Published on: July 12, 2019

Early mitochondrial dysfunction after cortical contusion injury.

Lesley K Gilmer¹, Kelly N Roberts, Kelly Joy

¹Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536-0230, USA.

Journal of Neurotrauma

|July 30, 2009

Summary

Traumatic brain injury impairs mitochondria, decreasing energy production. This study shows significant mitochondrial dysfunction within 1-3 hours post-injury, highlighting the need for early therapeutic intervention.

More Related Videos

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Related Experiment Videos

Last Updated: Jun 21, 2026

A Novel and Translational Rat Model of Concussion Combining Force and Rotation with In Vivo Cerebral Microdialysis

A Novel and Translational Rat Model of Concussion Combining Force and Rotation with In Vivo Cerebral Microdialysis

Published on: July 12, 2019

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Area of Science:

Neuroscience
Cellular Biology
Biochemistry

Background:

Traumatic brain injury (TBI) causes mitochondrial dysfunction, contributing to secondary brain damage.
Mitochondria are crucial for cellular energy production and neuronal survival.

Purpose of the Study:

To investigate mitochondrial bioenergetic changes in the rat neocortex at 1 and 3 hours after mild, moderate, and severe TBI.
To assess the impact of injury severity and time post-trauma on mitochondrial respiration and ATP production.

Main Methods:

Inducing unilateral cortical contusion injuries of varying severity in Sprague-Dawley rats.
Isolating synaptic and extrasynaptic mitochondria from injured and contralateral cortical tissue using differential centrifugation.
Assessing mitochondrial bioenergetics, including respiration, respiratory control ratio, and ATP production, using a Clark-type electrode.

Main Results:

Mitochondrial respiration was significantly impaired across all injury severity levels compared to uninjured controls.
Complex 1- and Complex 2-driven respirations were proportionally affected by injury severity.
Total oxygen utilization, respiratory control ratio, ATP production, and maximal respiration were significantly decreased in the injured cortex at 1 and 3 hours post-trauma.
Mitochondrial deficits observed at 1 hour were not exacerbated by 3 hours post-injury.

Conclusions:

TBI induces significant mitochondrial bioenergetic deficits in the neocortex.
These deficits occur early, within 1-3 hours post-injury, and are related to injury severity.
The findings underscore the critical window for early therapeutic interventions to mitigate secondary brain damage.