AI Article Synopsis
- Drugs of abuse, particularly cocaine, cause long-lasting changes in glutamatergic signaling, affecting communication between neurons in the brain's reward circuits.
- These alterations include shifts in glutamate concentrations, receptor function, and structural changes at synapses, which impact behavior related to cocaine use.
- The chapter will outline the neurocircuitry involved, detail glutamatergic neuroplasticity linked to cocaine addiction, and explore potential pharmacological treatments targeting glutamate for cocaine dependence.
Article Abstract
Neuroadaptations among glutamatergic projections within the mesocorticolimbic circuits engaged by drugs of abuse have been described since the 1990s. There is now substantial evidence that drugs of abuse lead to long-term changes in glutamatergic signaling and encompass multiple levels of analysis. For example, cocaine induces changes in extracellular glutamate concentrations and in synaptic glutamatergic transmission. In addition, glutamate receptors are required for the expression of cocaine-related behaviors, and long-term changes have been reported in the expression of proteins at glutamatergic synapses, in glutamate-related redox regulation of neurons, and in glutamatergic synaptic and structural plasticity following chronic exposure to cocaine. In this chapter, we will describe the neurocircuitry involved, and will summarize evidence for adaptations in glutamatergic neuroplasticity as a mechanism for cocaine addiction. Finally, we will discuss progress in the development of glutamate-mediated pharmacotherapies for the treatment of cocaine dependence.
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| http://dx.doi.org/10.1016/B978-0-12-385506-0.00009-0 | DOI Listing |
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