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Related Experiment Videos

Impact of basic FGF expression in astrocytes on dopamine neuron synaptic function and development.

Caroline Forget1, Jane Stewart, Louis-Eric Trudeau

  • 1Department of Pharmacology, Faculty of Medicine, Université de Montréal, C.P. 6128, Succursale Centre-Ville Montréal, Québec, Canada, H3C 3J7.

The European Journal of Neuroscience
|February 21, 2006
PubMed
Summary

Amphetamine sensitization involves midbrain dopamine neurons. Astrocytic basic fibroblast growth factor (bFGF) is implicated, but this study shows bFGF is not secreted, suggesting indirect glial-neuronal interactions enhance dopamine release.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Behavioural sensitization to amphetamine (AMPH) is linked to dopamine (DA) neurons in the ventral midbrain.
  • In vivo studies suggest enhanced expression of basic fibroblast growth factor (bFGF) in midbrain astrocytes contributes to AMPH sensitization.
  • A proposed mechanism involves AMPH-induced bFGF secretion by astrocytes, leading to long-term plasticity in DA neurons.

Purpose of the Study:

  • To directly investigate the effects of astrocytic basic fibroblast growth factor (bFGF) on dopamine (DA) neurons.
  • To elucidate the role of bFGF secretion versus nuclear expression in astrocyte-neuron interactions.
  • To understand the mechanisms underlying amphetamine (AMPH) sensitization in the ventral midbrain.

Main Methods:

Related Experiment Videos

  • Established a cell-culture model of mesencephalic astrocytes and DA neurons.
  • Utilized immunolabelling to assess bFGF expression in astrocytes.
  • Measured bFGF in the extracellular medium and assessed DA release and synapse formation.
  • Employed RNA interference (siRNA) against bFGF mRNA to evaluate its functional impact.

    • Main Results:

    • Mesencephalic astrocytes in culture express abundant nuclear bFGF under basal conditions.
    • bFGF was undetectable in the extracellular medium, indicating no significant secretion.
    • Exogenous bFGF altered astrocyte morphology, increased spontaneous DA release, and inhibited synapse formation.
    • siRNA-mediated reduction of bFGF decreased DA release but did not affect synaptic development.

    Conclusions:

    • Under basal conditions, bFGF is not secreted by astrocytes, despite high nuclear expression.
    • The observed effects of bFGF on DA neurons are likely mediated by indirect glial-neuronal interactions.
    • These interactions enhance DA release without necessarily altering synapse number, offering insights into AMPH sensitization mechanisms.