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Adrenergic nerve smooth endoplasmic reticulum calcium buffering declines with age
H Tsai1, W J Pottorf, J N Buchholz
1Department of Pharmacology, College of Medicine, University of California, Irvine 92697, USA.
Neurobiology of Aging
|April 30, 1998
Summary
Aging reduces smooth endoplasmic reticulum (SER) calcium buffering in sympathetic nerves. This age-related decline makes older nerves more reliant on mitochondria for calcium regulation.
Area of Science:
- Neuroscience
- Cell Biology
- Physiology
Background:
- Sympathetic nerve function is crucial for regulating cardiovascular parameters.
- Age-related changes in calcium homeostasis can impair nerve function.
- The role of smooth endoplasmic reticulum (SER) in age-related calcium buffering decline is not fully understood.
Purpose of the Study:
- To investigate the age-related functional decline of SER calcium buffering in sympathetic nerves.
- To determine the impact of SER calcium-ATPase inhibition on norepinephrine release and intracellular calcium dynamics in young versus aged rat sympathetic neurons.
Main Methods:
- Utilized rat tail artery sympathetic nerves and isolated superior cervical ganglion cells.
- Administered SER calcium-ATPase inhibitors (thapsigargin and cyclopiazonic acid).
- Measured norepinephrine release and intracellular calcium transients following K+-depolarization.
Main Results:
- SER calcium-ATPase inhibitors significantly increased norepinephrine release in young (6-month) but not old (20-month) rat tail arteries.
- In isolated neurons, these inhibitors enhanced the rate of calcium rise during depolarization only in young cells.
- In young cells, SER inhibitors altered calcium transient kinetics (time to peak, decline, time to basal), with no such effects observed in old cells.
Conclusions:
- Demonstrates an age-related decline in the functional capacity of SER calcium buffering mechanisms within the sympathetic nervous system.
- Suggests that older sympathetic nerves compensate by increasing reliance on mitochondrial calcium buffering.
- Highlights potential mechanisms underlying age-associated alterations in sympathetic neurotransmission and vascular control.
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