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Related Experiment Videos

Increased calcium buffering in basal forebrain neurons during aging

D Murchison1, W H Griffith

  • 1Department of Medical Pharmacology and Toxicology, College of Medicine, Texas A&M University Health Science Center, College Station, Texas 77843-1114, USA.

Journal of Neurophysiology
|July 11, 1998
PubMed
Summary

Aging neurons show increased calcium buffering to compensate for higher calcium influx, despite unchanged basal levels. This finding offers insights into age-related neural changes and potential dysfunction.

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Aging Research

Background:

  • Neuronal calcium (Ca2+) homeostasis is crucial for nervous system function and is implicated in age-related cognitive decline and diseases like Alzheimer's.
  • Basal forebrain neurons are particularly vulnerable to aging processes.
  • Previous studies indicated increased voltage-gated calcium channel (VGCC) influx in aged basal forebrain neurons.

Purpose of the Study:

  • To investigate age-related changes in calcium buffering mechanisms within basal forebrain neurons.
  • To determine if altered calcium buffering contributes to the increased calcium influx observed in aged neurons.

Main Methods:

  • Utilized whole-cell and perforated-patch voltage clamp techniques combined with fura-2 microfluorimetry.
  • Quantified basal intracellular Ca2+ concentrations, Ca2+ influx, and Ca2+ transients (Delta[Ca2+]i).

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  • Assessed the role of the smooth endoplasmic reticulum (SER) using thapsigargin, a SER Ca2+ uptake blocker.

    • Main Results:

    • Observed an age-related increase in rapid calcium buffering and the time course of Ca2+ transients (Delta[Ca2+]i).
    • Basal intracellular Ca2+ concentrations ([Ca2+]i) remained unchanged between young and aged rats.
    • Neither the SER nor endogenous diffusible buffering mechanisms fully explained the observed age-related increase in buffering.

    Conclusions:

    • Aging central neurons may exhibit enhanced calcium buffering as a compensatory mechanism for increased Ca2+ influx.
    • This compensatory buffering may help maintain neuronal function despite age-associated alterations in calcium homeostasis.
    • Further research is needed to elucidate the precise molecular mechanisms underlying this age-related increase in calcium buffering.