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Electron microscopy techniques employed to explore mitochondrial defects in the developing rat brain following
Trisha Eustaquio1, Cheng Wang2, Christopher K Dugard1
1NCTR/ORA Nanotechnology Core Facility, Office of Scientific Coordination, National Center for Toxicological Research, US Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, United States.
Experimental Cell Research
|October 21, 2018
Summary
Ketamine exposure causes mitochondrial swelling and potential fission in developing rat brains. These ultrastructural changes support ketamine
Area of Science:
- Neuroscience
- Cell Biology
- Toxicology
Background:
- Ketamine, an NMDA receptor antagonist, is used in pediatric anesthesia.
- Prolonged ketamine exposure may cause neurotoxicity in developing brains.
- Mitochondrial role in cell death is known, but ultrastructural changes from ketamine are unclear.
Purpose of the Study:
- To investigate ketamine's impact on mitochondrial ultrastructure in the developing rat brain.
- To utilize transmission electron microscopy (TEM) and serial block-face scanning electron microscopy (SBF-SEM).
Main Methods:
- Postnatal day 7 rats received ketamine or saline injections.
- Frontal cortex samples were analyzed using TEM and SBF-SEM.
- Mitochondrial morphology and 3D reconstructions were evaluated.
Main Results:
- Ketamine exposure induced significant mitochondrial swelling.
- SBF-SEM revealed 3D mitochondrial swelling and potential fission.
- Ketamine-treated mitochondria showed larger volumes per unit surface area.
Conclusions:
- TEM and SBF-SEM demonstrated ultrastructural mitochondrial alterations.
- These changes support ketamine's neurotoxicity mechanism in developing brains.
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