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Related Experiment Videos

Glutamate receptor agonists decrease extracellular dopamine in the rat nucleus accumbens in vivo

M T Taber1, G B Baker, H C Fibiger

  • 1Department of Psychiatry, University of British Columbia, Vancouver, Canada.

Synapse (New York, N.Y.)
|October 1, 1996
PubMed
Summary
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Glutamate receptor agonists in the nucleus accumbens can increase or decrease dopamine release. However, inhibiting glutamate uptake primarily inhibits dopamine release, suggesting a complex, multisynaptic interaction.

Area of Science:

  • Neuroscience
  • Neurochemistry

Background:

  • The nucleus accumbens (NAc) is a key brain region involved in reward and motivation.
  • Dopamine (DA) signaling in the NAc is modulated by glutamate, the primary excitatory neurotransmitter.

Purpose of the Study:

  • To investigate the effects of L-glutamate, N-methyl-D-aspartate (NMDA), and a glutamate uptake inhibitor (PDC) on extracellular dopamine in the NAc.
  • To examine the impact of PDC on extracellular glutamate concentrations.

Main Methods:

  • Intracerebral microdialysis in the NAc.
  • Local application of L-glutamate, NMDA, PDC, and kynurenic acid (KYN).
  • Measurement of extracellular dopamine and glutamate concentrations.

Main Results:

Related Experiment Videos

  • Glutamate decreased extracellular DA in a concentration-dependent manner, blocked by KYN.
  • NMDA showed concentration-dependent effects on DA release (decrease at low, increase at high concentrations), both blocked by KYN.
  • PDC increased extracellular glutamate and decreased extracellular DA, an effect attenuated by KYN.
  • Glutamate's inhibitory effects on DA release in the NAc are likely mediated by a multisynaptic pathway, not direct action on DA terminals.

    • Conclusions:

    • Glutamate receptor agonists exert both inhibitory and facilitatory effects on NAc dopamine release.
    • Inhibition of dopamine release by PDC suggests this is a more physiologically relevant effect.
    • Glutamate's inhibitory actions on NAc dopamine are mediated via indirect, multisynaptic mechanisms.