Dichotomous dopaminergic control of striatal synaptic plasticity
Open accessAbstract
At synapses between cortical pyramidal neurons and principal striatal medium spiny neurons (MSNs), postsynaptic D1 and D2 dopamine (DA) receptors are postulated to be necessary for the induction of long-term potentiation and depression, respectively—forms of plasticity thought to underlie associative learning. Because these receptors are restricted to two distinct MSN populations, this postulate demands that synaptic plasticity be unidirectional in each cell type. Using brain slices from DA receptor transgenic mice, we show that this is not the case. Rather, DA plays complementary roles in these two types of MSN to ensure that synaptic plasticity is bidirectional and Hebbian. In models of Parkinson's disease, this system is thrown out of balance, leading to unidirectional changes in plasticity that could underlie network pathology and symptoms.
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Larger NMDA currents may enhance the probability of plasticity because NMDA receptors drive spike-timing dependent calcium-dependent potentiation on medium spiny neuron subtypes.
“Additionally, these synapses display larger NMDA currents which may enhance the probability of plasticity as NMDA receptors drive spike-timing dependent calcium-dependent potentiation on MSN subtypes (50).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [50]
Ventral hippocampal to nucleus accumbens synapses display larger NMDA currents.
“Additionally, these synapses display larger NMDA currents which may enhance the probability of plasticity as NMDA receptors drive spike-timing dependent calcium-dependent potentiation on MSN subtypes (50).”
From Emerging Role for Nucleus Accumbens Medium Spiny Neuron Subtypes in Depression (2017) · cites this paper as [50]
Impaired neuroplasticity under dopamine denervation may give rise to aberrant learning that further impairs automatic motor behavior.
“which may give rise to an aberrant learning that further impairs automatic motor behavior 45, 46.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [45]
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- Authors
- Shen, W., Flajolet, M., Greengard, P., & Surmeier, D. J.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Surmeier, D. James
- Venue
- Science
- Published
- 2008-08-08
- Volume
- 321
- Issue
- 5890
- Pages
- 848-851
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2833421
- OpenAlex
- W1971999279
- Cited by
- 1,190
- References
- 29
- Citations by year
- 2026: 43 · 2025: 53 · 2024: 46 · 2023: 58 · 2022: 59 · 2021: 72 · 2020: 64 · 2019: 61 · 2018: 81 · 2017: 68 · 2016: 65 · 2015: 71 · 2014: 61 · 2013: 69 · 2012: 74
- FWCI
- 35.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (MH-074866, P50MH074866)
- National Institute on Drug Abuse (DA10044, P01DA010044)
- National Institute of Neurological Disorders and Stroke (NS 34696, R01NS034696, R37NS034696)
- 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, striatum, medium spiny neurons, synaptic plasticity, dopamine D1 receptor, dopamine D2 receptor, long-term potentiation, long-term depression, bidirectional plasticity, Hebbian learning, Parkinson's disease
- MeSH terms
- Animals, Corpus Striatum, Dopamine, Mice, Transgenic, Neurons, Synapses, Signal Transduction, Receptors, Dopamine D1, Receptors, Dopamine D2, Long-Term Potentiation, Glutamic Acid, Parkinsonian Disorders, Long-Term Synaptic Depression, Mice, Cannabinoid Receptor Modulators
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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