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Neuromuscular transmission modulation by adenosine upon aging.

Paula A Pousinha1, Alexandra M Correia, Ana M Sebastião

  • 1Institute of Pharmacology and Neurosciences, Faculty of Medicine, University of Lisbon, Portugal.

Neurobiology of Aging
|February 28, 2012
PubMed
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Aging reduces the facilitatory effects of adenosine A(2A) receptors on neuromuscular transmission in rats. Inhibitory A1 receptor effects remain unchanged, suggesting A(2A) receptor decline contributes to age-related functional changes.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Aging Research

Background:

  • Adenosine receptors modulate neuromuscular transmission.
  • A(2A) receptor-mediated effects predominate in infant rats.
  • The impact of aging on this receptor balance is unknown.

Purpose of the Study:

  • To investigate how aging affects the balance of adenosine A(2A) and A1 receptor modulation of neuromuscular transmission.
  • To determine if age-related changes occur in presynaptic adenosine receptor function.

Main Methods:

  • Recorded evoked (EPPs) and miniature end plate potentials (MEPPs) in rat diaphragm muscle fibers across different age groups (infant, young adult, older, aged).
  • Utilized selective and non-selective adenosine receptor agonists and antagonists to probe receptor function.
  • Administered 2-chloroadenosine (CADO), iodotubericidin (ITU), ZM241385, CGS21680, and 6-cyclopentyladenosine (CPA).

Main Results:

  • Adenosine A(2A) receptor-mediated facilitation of EPPs (amplitude and quantal content) was observed in infant, young adult, and older rats but absent in aged rats.
  • A1 receptor-mediated inhibition of EPP amplitude was consistent across all age groups.
  • Facilitatory effects were blocked by A(2A) antagonist ZM241385 and mimicked by A(2A) agonist CGS21680.

Conclusions:

  • Aging differentially impacts adenosine A(2A) and A1 receptor-mediated presynaptic modulation of neuromuscular transmission.
  • The facilitatory influence of A(2A) receptors decreases with age, while inhibitory A1 receptor effects remain stable.
  • Reduced adenosine A(2A) receptor function may contribute to age-related neuromuscular decline.