Dopamine-mediated regulation of corticostriatal synaptic plasticity
Abstract
The striatum represents the main input into the basal ganglia. Neurons projecting from the striatum receive a large convergence of afferents from all areas of the cortex and transmit neural information to the basal ganglia output structures. Corticostriatal transmission is essential in the regulation of voluntary movement, in addition to behavioural control, cognitive function and reward mechanisms. Long-term potentiation (LTP) and long-term depression (LTD), the two main forms of synaptic plasticity, are both represented at corticostriatal synapses and strongly depend on the activation of dopamine receptors. Here, we discuss possible feedforward and feedback mechanisms by which striatal interneurons, in association with striatal spiny neurons and endogenous dopamine, influence the formation and maintenance of both LTP and LTD. We also propose a model in which the spontaneous membrane oscillations of neurons projecting from the striatum (named 'up' and 'down' states), in addition to the pattern of release of endogenous dopamine, bias the synapse towards preferential induction of LTP or LTD. Finally, we discuss how endogenous dopamine crucially influences changes in synaptic plasticity induced by pathological stimuli, such as energy deprivation.
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Cortico-striatal synapses can undergo both long-term potentiation and long-term depression.
“Cortico-striatal synapses can undergo both strengthening (long-term potentiation, or LTP), and weakening (long-term depression, or LTD; [32–33]).”
From Cortical and basal ganglia contributions to habit learning and automaticity (2010) · cites this paper as [32]
Cortical high-frequency stimulation has most frequently been observed to produce long-term depression at cortico-striatal synapses.
“Cortical high-frequency stimulation has most frequently been observed to produce LTD at cortico-striatal synapses.”
From Cortical and basal ganglia contributions to habit learning and automaticity (2010) · cites this paper as [32]
Dopamine depletion in the striatum leads to loss of dendritic spines on striatal medium spiny neurons in animal models and in Parkinson's disease.
“DA-depletion in the striatum leads to the loss of dendritic spines on striatal medium spiny neurons (MSNs) in both animal models87–89 and in PD90.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [88]
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“Because striatal dopamine (DA) release is critical for LTP induction in this brain structure (Calabresi et al., 2007) and based on the evidence that striatal LTP depends on E2 local synthesis, the interaction between E2 and DA in controlling SPNs’ LTP was explored.”
BackgroundSelf-citationWhat does the habenula tell dopamine neurons?
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- Authors
- Calabresi, P., Picconi, B., Tozzi, A., & Di Filippo, M.
- Affiliations
- University of Perugia (IT)
- Fondazione Santa Lucia (IT)
- Corresponding author
- Calabresi, Paolo
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 30
- Issue
- 5
- Pages
- 211-219
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W2058077554
- Cited by
- 865
- References
- 74
- Citations by year
- 2026: 31 · 2025: 47 · 2024: 33 · 2023: 33 · 2022: 37 · 2021: 48 · 2020: 68 · 2019: 30 · 2018: 25 · 2017: 39 · 2016: 34 · 2015: 56 · 2014: 47 · 2013: 53 · 2012: 43
- FWCI
- 5.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- 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, corticostriatal synapses, synaptic plasticity, long-term potentiation, long-term depression, striatal interneurons, endogenous dopamine release, up-down states, membrane potential oscillations, basal ganglia, energy deprivation
- MeSH terms
- Animals, Corpus Striatum, Dopamine, Humans, Neural Pathways, Neuronal Plasticity, Synapses
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