Altered AMPA receptor expression with treadmill exercise in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse model of basal ganglia injury
Abstract
Dopamine depletion leads to impaired motor performance and increased glutamatergic-mediated hyperexcitability of medium spiny neurons in the basal ganglia. Intensive treadmill exercise improves motor performance in both saline treatment and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In the present study, we investigated the effect of high-intensity treadmill exercise on changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunit expression, because these receptor channels confer the majority of fast excitatory neurotransmission in the brain, and their subunit composition provides a key mechanism for regulating synaptic strength and synaptic neuroplasticity and is important in modulating glutamatergic neurotransmission. Within the dorsolateral striatum of MPTP mice, treadmill exercise increased GluR2 subunit expression, with no significant effect on GluR1. Furthermore, neurophysiological studies demonstrated a reduction in the size of excitatory postsynaptic currents (EPSCs) in striatal medium spiny neurons (as determined by the input-output relationship), reduced amplitude of spontaneous EPSCs, and a loss of polyamine-sensitive inward rectification, all supportive of an increase in heteromeric AMPAR channels containing the GluR2 subunit. Phosphorylation of GluR2 at serine 880 in both saline-treated and MPTP mice suggests that exercise may also influence AMPAR trafficking and thus synaptic strength within the striatum. Finally, treadmill exercise also altered flip isoforms of GluR2 and GluR1 mRNA transcripts. These findings suggest a role for AMPARs in mediating the beneficial effects of exercise and support the idea that adaptive changes in GluR2 subunit expression may be important in modulating experience-dependent neuroplasticity of the injured basal ganglia.
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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 [89]
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- Authors
- VanLeeuwen, J., Petzinger, G. M., Walsh, J. P., Akopian, G. K., Vuckovic, M., & Jakowec, M. W.
- Affiliations
- University of Southern California (US)
- Corresponding author
- Petzinger, Giselle M.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2009-09-10
- Volume
- 88
- Issue
- 3
- Pages
- 650-668
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W1971168591
- Cited by
- 94
- References
- 87
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 10 · 2019: 7 · 2018: 4 · 2017: 13 · 2016: 5 · 2015: 8 · 2014: 4 · 2013: 9 · 2012: 5
- FWCI
- 1.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01 AG 21937, R01AG021937)
- National Institute of Neurological Disorders and Stroke (R01NS044327, R01 NS44327-1)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- AMPA receptors, GluR2 subunit, GluR1 subunit, treadmill exercise, MPTP mouse model, Parkinson's disease, basal ganglia lesions, dorsolateral striatum, medium spiny neurons, excitatory postsynaptic currents, inward rectification, neuroplasticity, dopamine depletion
- MeSH terms
- Animals, Basal Ganglia, Corpus Striatum, Disease Models, Animal, Dopamine, Male, Membrane Potentials, Mice, Inbred C57BL, Neurons, Parkinson Disease, Secondary, Physical Conditioning, Animal, Random Allocation, RNA, Messenger, Synapses, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Receptors, AMPA, Excitatory Postsynaptic Potentials, Protein Isoforms, Mice
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.
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