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Intracellular calcium deposition in brain following electrical stimulation
Neurological Research
|January 1, 1979
Summary
Electrical stimulation of the cat cerebral cortex caused calcium hydroxyapatite crystal buildup. This intracellular calcification correlated with neuronal damage and cell death in stimulated brain tissue.
Area of Science:
- Neuroscience
- Biomaterials Science
- Cell Biology
Background:
- Electrical stimulation is used therapeutically for neurological conditions.
- Understanding the cellular effects of electrical stimulation is crucial for optimizing treatment.
- Previous studies have not fully elucidated the ultrastructural changes induced by chronic electrical stimulation.
Purpose of the Study:
- To investigate the cellular and ultrastructural effects of chronic electrical stimulation on the cat cerebral cortex.
- To identify the nature of crystalline inclusions observed in stimulated neurons.
- To explore the relationship between electrical stimulation parameters and tissue degeneration.
Main Methods:
- Bilateral subdural implantation of platinum or rhodium disc electrodes on the parietal cortex of cats.
- Application of electrical stimulation with varying parameters (10 - 300 μC/cm²/ph) for 36 hours over 4 days.
- Evaluation of tissue changes using light and electron microscopy, including electron diffraction and energy-dispersive X-ray analysis.
Main Results:
- Dense crystalline inclusions identified as calcium hydroxyapatite (CHA) crystals were observed in stimulated cortical tissue.
- Intracellular calcification, particularly in mitochondria and postsynaptic dendrites, paralleled degenerative changes like gliosis, mitochondrial swelling, and neuronal loss.
- Phagocytic activity and degenerating cells were prominent in stimulated areas.
Conclusions:
- Chronic electrical stimulation of the cat cerebral cortex can lead to intracellular calcium hydroxyapatite deposition.
- This calcification is associated with significant neuronal and cellular degeneration.
- The findings suggest a potential mechanism involving increased cyclic AMP and enhanced calcium permeability, though the precise electroresponsive mechanism requires further investigation.