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Subcellular Imaging of Neuronal Calcium Handling In Vivo
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Age-dependent changes in Ca2+ homeostasis in peripheral neurones: implications for changes in function.

John N Buchholz1, Erik J Behringer, William J Pottorf

  • 1Department of Physiology and Pharmacology, Loma Linda University, School of Medicine, Loma Linda, CA 92350, USA. jbuchholz@llu.edu

Aging Cell
|May 23, 2007
PubMed
Summary

Aging subtly impacts peripheral neurons, altering intracellular calcium ([Ca2+]i) regulation. Neurons compensate for declining calcium ATPases by enhancing mitochondrial and plasmalemma buffering, but increased mitochondrial uptake may risk cell death.

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13:24

Fluorescence and Bioluminescence Imaging of Subcellular Ca2+ in Aged Hippocampal Neurons

Published on: December 1, 2015

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Aging Research

Background:

  • Calcium ions are crucial second messengers in neuronal cells, regulating vital functions like neurotransmitter release and cell death.
  • Intracellular calcium ([Ca2+]i) transients are precisely controlled by complex regulatory mechanisms.
  • Disruptions in calcium regulation can impact peripheral neuron health, particularly during aging.

Purpose of the Study:

  • To review the impact of aging on peripheral adrenergic neuron function.
  • To explore the link between age-related functional changes and alterations in intracellular calcium ([Ca2+]i) regulation.
  • To examine compensatory mechanisms in neuronal calcium buffering with age.

Main Methods:

  • Literature review focusing on studies investigating aging effects on peripheral autonomic neurons.
  • Analysis of research on intracellular calcium ([Ca2+]i) regulation and its modulation in aging neurons.
  • Examination of data on calcium-buffering systems including smooth endoplasmic reticulum calcium ATPases, mitochondria, and plasmalemma calcium extrusion.

Main Results:

  • Normal aging in peripheral autonomic neurons is often subtle, not always leading to severe functional decline.
  • Neurons can compensate for age-related decreases in smooth endoplasmic reticulum calcium ATPase function by upregulating mitochondrial and plasmalemma calcium buffering.
  • Increased mitochondrial calcium uptake may pose a risk for neuronal viability over time.
  • Age-related alterations in calcium release from smooth endoplasmic reticulum stores involve changes in ryanodine receptor levels and modulation by nitric oxide.

Conclusions:

  • Peripheral neurons exhibit compensatory strategies for age-related calcium dysregulation to maintain viability.
  • While compensatory mechanisms exist, increased reliance on mitochondrial calcium uptake may represent a vulnerability.
  • Age-associated changes in calcium release mechanisms, influenced by ryanodine receptors and nitric oxide, further complicate neuronal calcium homeostasis.