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Influence of age on BDNF modulation of hippocampal synaptic transmission: interplay with adenosine A2A receptors

Maria J Diógenes1, Natália Assaife-Lopes, António Pinto-Duarte

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

Hippocampus
|April 11, 2007
PubMed

Insights

Adenosine A(2A) receptor activation potentiates brain-derived neurotrophic factor (BDNF) synaptic actions in young and aged rats. Age-related receptor changes influence BDNF

Area of Science:

  • Neuroscience
  • Neurobiology
  • Synaptic Plasticity

Background:

  • Adenosine A(2A) receptor activation potentiates brain-derived neurotrophic factor (BDNF) synaptic actions in infant rat hippocampus.
  • A(2A)-receptor-mediated actions are more pronounced in older rats, suggesting therapeutic potential for BDNF strategies in aging subjects.

Purpose of the Study:

  • To evaluate the synaptic actions of BDNF and receptor levels (TrkB, adenosine A(2A)) in the hippocampus across different age groups of rats.
  • To investigate age-related variations in BDNF's effects on synaptic transmission.

Main Methods:

  • Electrophysiological recordings of field excitatory postsynaptic potentials (fEPSPs) in rat hippocampal slices.
  • Western blot analysis to determine TrkB receptor density.
  • Ligand binding assays to quantify adenosine A(2A) receptor levels.
  • Administration of BDNF and the A(2A) receptor antagonist ZM 241385.

Main Results:

  • BDNF enhanced synaptic transmission in young adult and aged rats, an effect mediated by adenosine A(2A) receptor activation.
  • BDNF showed minimal effect on synaptic transmission in infant and old adult rats.
  • TrkB receptor levels decreased in old adult and aged rats.
  • Adenosine A(2A) receptor levels increased in the hippocampus of old adult and aged rats.

Conclusions:

  • Age-related alterations in TrkB and adenosine A(2A) receptor densities contribute to non-monotonic variations in BDNF's synaptic actions.
  • Understanding these age-dependent changes is crucial for developing effective BDNF-based therapeutic strategies for cognitive aging.

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