Synaptic plasticity and physiological interactions between dopamine and glutamate in the striatum
Abstract
Several electrophysiological studies have addressed the interaction between glutamate and dopamine within the striatum. Although the results obtained from these studies were often conflicting, more recently the characterization of new forms of synaptic plasticity in the basal ganglia provided a possible integrative explanation of the different electrophysiological data regarding the interaction between these transmitters. In this review we will try to summarize and discuss the available data concerning the possible impact of the functional role of D1 and D2 receptor activation on the modulation of the glutamatergic corticostriatal pathway. Moreover, we will also describe the function of the striatum in the integration of glutamatergic and dopaminergic inputs to produce long-term changes of synaptic efficacy (long-term depression, long-term potentiation). Finally, we will consider the implication of the interaction between dopamine and glutamate in the regulation of energetic metabolism whose failure is responsible for neuronal death.
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Accumulating evidence suggests neuroplasticity within the corticostriatal circuit is impaired under conditions of dopamine denervation.
“However, accumulating evidence suggest that neuroplasticity within this corticostriatal circuit is also impaired under conditions of DA denervation 41–44”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [44]
Exercise can alter the storage and release of glutamate in presynaptic terminals that may improve circuit function and diminish the increased inhibitory drive of the dopamine depleted striatum.
“In addition to its receptors, exercise can also alter the storage and release of glutamate in presynaptic terminals that may also improve circuit function and diminish the increased inhibitory drive of the DA depleted striatum 41–44.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [44]
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- Authors
- Calabresi, P., Pisani, A., Centonze, D., & Bernardi, G.
- Affiliations
- University of Rome Tor Vergata (IT)
- Fondazione Santa Lucia (IT)
- Corresponding author
- Calabresi, P.
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 1997-01
- Volume
- 21
- Issue
- 4
- Pages
- 519-523
- ISSN
- 0149-7634 (ISSN-L)
- OpenAlex
- W1970320255
- Cited by
- 117
- References
- 62
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 2 · 2020: 4 · 2019: 2 · 2018: 1 · 2017: 3 · 2015: 3 · 2014: 5 · 2013: 7 · 2012: 2
- FWCI
- 2.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Funders
- Centre National de la Recherche Scientifique
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- dopamine-glutamate interaction, striatum, synaptic plasticity, dopamine D1 receptor, dopamine D2 receptor, corticostriatal pathway, long-term depression, long-term potentiation, basal ganglia, energy metabolism, neuronal cell death
- MeSH terms
- Animals, Dopamine, Humans, Neuronal Plasticity, Synapses, Neostriatum, Receptors, Glutamate, Glutamic Acid
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