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Related Experiment Videos

Calcium chelation improves spatial learning and synaptic plasticity in aged rats.

Alexander Tonkikh1, Christopher Janus, Hossam El-Beheiry

  • 1Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada.

Experimental Neurology
|July 26, 2005
PubMed
Summary
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Elevated intracellular calcium impairs brain plasticity and learning in aging. Chelating calcium with BAPTA-AM improved synaptic plasticity and spatial learning in aged rats, suggesting a therapeutic target for cognitive decline.

Area of Science:

  • Neuroscience
  • Calcium Signaling
  • Aging Brain Research

Background:

  • Intracellular calcium dysregulation is linked to cognitive deficits and impaired synaptic plasticity in aged brains.
  • Aged Fisher 344 rats exhibit reduced synaptic responses and diminished long-term potentiation (LTP) in hippocampal slices.
  • Elevated resting calcium levels are observed in presynaptic terminals of aged rat hippocampal slices.

Purpose of the Study:

  • To investigate the role of intracellular calcium in age-related cognitive decline and synaptic plasticity.
  • To determine if modulating intracellular calcium levels can rescue cognitive and plasticity deficits in aged rats.

Main Methods:

  • Electrophysiological recordings of CA1 field EPSPs and LTP in hippocampal slices from young and aged rats.

Related Experiment Videos

  • Measurement of resting intracellular calcium levels in presynaptic terminals.
  • Administration of BAPTA-AM (a calcium chelator) in vitro and in vivo.
  • Behavioral testing using the Morris water maze to assess spatial learning in rats.

    • Main Results:

    • Aged rats showed smaller CA1 field EPSPs and impaired LTP compared to young rats.
    • Presynaptic terminals in aged rats had elevated resting calcium levels.
    • BAPTA-AM depressed LTP in young slices but enhanced it in aged slices.
    • In vivo BAPTA-AM administration improved spatial learning acquisition in aged rats but not young rats.

    Conclusions:

    • Increased intracellular neuronal calcium buffering, achieved with BAPTA-AM, ameliorates age-related deficits in synaptic plasticity.
    • Modulating intracellular calcium levels offers a potential strategy to counteract age-related cognitive impairment and synaptic dysfunction.