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Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
Published on: November 21, 2013
Calcium transport abnormality in uremic rat brain synaptosomes
The Journal of Clinical Investigation
|November 1, 1985
Summary
Uremia increases brain calcium by enhancing two key transport mechanisms in nerve endings. These changes in calcium transport may impact neurotransmission in uremic patients.
Area of Science:
- Neuroscience
- Nephrology
- Biochemistry
Background:
- Elevated brain calcium is observed in uremia, but its functional significance remains unclear.
- Uremia is a complex condition characterized by the buildup of waste products in the blood.
- Calcium homeostasis plays a critical role in neuronal function.
Purpose of the Study:
- To investigate the mechanisms of calcium transport in the brain of rats with acute uremia.
- To determine if uremia affects specific calcium transport pathways in cerebral cortex synaptosomes.
- To elucidate the impact of uremia on calcium influx and efflux in brain nerve endings.
Main Methods:
- Utilized synaptosomes from the cerebral cortex of normal and acutely uremic rats.
- Employed radioactive 45Ca++ to trace calcium transport.
- Assessed Na+-Ca++ exchange and ATP-dependent calcium uptake in isolated synaptosomes and vesicles.
Main Results:
- Significantly increased calcium accumulation via Na+-Ca++ exchange in uremic rat synaptosomes.
- Significantly elevated ATP-dependent calcium uptake in synaptosomes from uremic rats.
- These findings suggest increased synaptosomal membrane permeability to calcium in uremia.
Conclusions:
- Uremia enhances both Na+-Ca++ exchange and ATP-dependent calcium transport in brain synaptosomes.
- Increased calcium transport in uremia may lead to elevated extracellular brain calcium.
- Observed calcium transport defects in uremia are not readily reversible and may affect neurotransmission.
