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Glutamate-dopamine cotransmission and reward processing in addiction
Christopher C Lapish1, Jeremy K Seamans, L Judson Chandler
1Department of Neurosciences and the Center for Drug and Alcohol Programs, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Alcoholism, Clinical and Experimental Research
|August 26, 2006
Summary
Classical neurotransmitter corelease is widespread. Glutamate and dopamine (DA) corelease, though controversial, may explain addiction by signaling reward prediction errors and modulating neuronal activity.
Area of Science:
- Neuroscience
- Neurobiology
- Addiction Research
Background:
- Dale's principle (one neuron, one neurotransmitter) is evolving.
- Corelease of atypical neurotransmitters (e.g., neuropeptides) is established.
- Corelease of classical neurotransmitters is increasingly recognized in the mammalian central nervous system.
Purpose of the Study:
- Review evidence for and against glutamate-dopamine (DA) cotransmission.
- Discuss the role of glutamate-DA corelease in addiction neurocircuitry.
- Explore implications for cognitive and reward processes.
Main Methods:
- Literature review and synthesis of existing studies.
- Analysis of evidence supporting and refuting glutamate-DA cotransmission.
- Discussion of a proposed model for glutamate-DA corelease function.
Main Results:
- Evidence suggests neurotransmitter corelease is widespread, involving most classical systems.
- Glutamate-DA cotransmission remains controversial but is supported by emerging data.
- A model proposes coreleased glutamate signals reward prediction errors, while DA provides prolonged modulation.
Conclusions:
- Glutamate-DA corelease has significant implications for understanding reward and cognition.
- This cotransmission may be crucial in the neurobiology of addiction.
- Alcohol addiction may involve a shift in the reward valence signal from positive to negative.
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