Related Experiment Video
Updated: May 24, 2026
07:47
Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy
Published on: July 9, 2016
Mitochondria and perinatal brain injury
Catherine I Rousset1, Ana A Baburamani, Claire Thornton
1Centre for the Developing Brain, Institute of Reproductive and Developmental biology, Department of Surgery & Cancer, Imperial College, Hammersmith Campus, London, UK.
Summary
Mitochondrial dysfunction contributes to brain injury after hypoxia-ischemia by disrupting energy production and triggering cell death. Mitochondrial dynamics are crucial for both brain development and cell fate decisions post-injury.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Secondary brain injury following hypoxia-ischemia involves delayed high-energy phosphate loss, suggesting mitochondrial bioenergetic failure.
- Deregulation of adenosine monophosphate-activated protein kinase (AMPK) and a toxic intracellular environment (reactive oxygen species, calcium) contribute to cell death pathways.
- Mitochondrial permeabilization (MP) is triggered by post-ischemic reperfusion, leading to caspase-dependent and apoptosis-inducing factor-dependent cell death, but the induction mechanism remains unclear.
Purpose of the Study:
- To review the critical role of mitochondria in immature central nervous system (CNS) development.
- To update the understanding of mitochondria's role in determining cell fate after hypoxia-ischemia in the immature CNS.
Main Methods:
- This review synthesizes existing research on mitochondrial function, dynamics, and their implications in brain development and injury.
- Focuses on the interplay between energy metabolism, oxidative stress, calcium homeostasis, and cell death pathways.
Main Results:
- Mitochondrial dynamics, including fusion and fission, are essential for normal brain development; deficiencies lead to malformations like microcephaly and dysmyelination.
- Mitochondrial bioenergetic failure, partly due to AMPK deregulation, is implicated in secondary brain injury after hypoxia-ischemia.
- Mitochondrial permeabilization is a key event in post-ischemic cell death, influenced by mitochondrial dynamics.
Conclusions:
- Mitochondria play a pivotal role in both the development of the immature brain and the cellular response to hypoxic-ischemic injury.
- Understanding mitochondrial dynamics and bioenergetics is crucial for developing therapeutic strategies for neonatal brain injury.
Related Concept Videos
01:27Protein Import into the Peroxisomes
Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
02:59Animal Mitochondrial Genetics
Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...