Striatal Akt/GSK3 signaling pathway in the development of L-Dopa-induced dyskinesias in MPTP monkeys
Abstract
L-Dopa treatment, the gold standard therapy for Parkinson's disease, is hampered by motor complications such as dyskinesias. Recently, impairment of striatal Akt/GSK3 signaling was proposed to play a role in the mechanisms implicated in development of L-Dopa-induced dyskinesias in a rodent model of Parkinson's disease. The present experiment investigated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys, the effects on Akt/GSK3 of chronic L-Dopa treatment inducing dyskinesias compared to L-Dopa with CI-1041 (NMDA receptor antagonist) or a low dose of cabergoline (dopamine D2 receptor agonist) preventing dyskinesias. The extensive dopamine denervation induced by MPTP was associated with a decrease by about half of phosphorylated Akt(Ser473) levels in posterior caudate nucleus, anterior and posterior putamen; smaller changes were observed for phosphorylated Akt(Thr308) levels that did not reach statistical significance. Dopamine depletion reduced phosphorylated GSK3beta(Ser9) levels, mainly in posterior putamen whereas pGSK3beta(Tyr216) and pGSK3alpha(Ser21) were unchanged. In posterior caudate nucleus, anterior and posterior putamen of dyskinetic L-Dopa-treated MPTP monkeys, pAkt(Ser473) and pGSK3beta(Ser9) were elevated whereas L-Dopa+cabergoline treated MPTP monkeys without dyskinesias had lower values in posterior striatum as vehicle-treated MPTP monkeys. In non-dyskinetic MPTP monkeys treated with L-Dopa+CI-1041, putamen pAkt(Ser473) and pGSK3beta(Ser9) levels remained elevated as in dyskinetic monkeys while in posterior caudate nucleus, these levels were low as vehicle-treated and lower than L-Dopa treated MPTP monkeys. Extent of phosphorylation of Akt and GSK3beta in putamen correlated positively with dyskinesias scores of MPTP monkeys; these correlations were higher with dopaminergic drugs (L-Dopa, cabergoline) suggesting implication of additional mechanisms and/or signaling molecules in the NMDA antagonist antidyskinetic effect. In conclusion, our results showed that in MPTP monkeys, loss of striatal dopamine decreased Akt/GSK3 signaling and that increased phosphorylation of Akt and GSK3beta was associated with L-Dopa-induced dyskinesias.
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AKT can promote neuronal survival by mediating multiple neurotrophic factors.
“as AKT can promote neuronal survival by mediating multiple neurotrophic factors (Morissette et al. 2010).”
From Therapeutic effect of GLP-1 engineered strain on mice model of Alzheimer’s disease and Parkinson’s disease (2020) · cites this paper as Morissette et al. 2010
P-AKT is a major anti-apoptotic kinase, so AKT/GSK3β signaling abnormalities are associated with many neurological diseases.
“P-AKT is a major anti-apoptotic kinase, so AKT/GSK3β signaling abnormalities are associated with many neurological diseases (Morissette et al. 2010).”
From Therapeutic effect of GLP-1 engineered strain on mice model of Alzheimer’s disease and Parkinson’s disease (2020) · cites this paper as Morissette et al. 2010
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Selenoprotein W Mitigates 6‐ OHDA ‐Induced Dopaminergic Damage and Motor Dysfunction in Mice
Kan, H.-Y., Zhang, F., Qiu, X., Wang, Z., Zeng, Z., Li, S., Chen, L., Ovlyakulov, B., Cui, L., Zhang, X., et al. (2026) · The FASEB Journal · doi:10.1096/fj.202603178r
- Authors
- Morissette, M., Samadi, P., Tahar, A. H., Bélanger, N., & Di Paolo, T.
- Affiliations
- Centre hospitalier universitaire de Québec (CA)
- Université Laval (CA)
- ORCID
- Morissette, Marc
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 34
- Issue
- 3
- Pages
- 446-454
- ISSN
- 0278-5846 (ISSN-L)
- OpenAlex
- W2070775710
- Cited by
- 47
- References
- 52
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 6 · 2013: 7 · 2012: 4
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Applied Materials
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- Parkinson's disease, GSK3β phosphorylation, Akt phosphorylation, dopamine depletion, NMDA receptor antagonists, cabergoline, caudate nucleus, putamen, antidyskinetic effect, dopamine D2 receptor agonist
- MeSH terms
- Cabergoline, Animals, Antiparkinson Agents, Benzoxazoles, Corpus Striatum, Disease Models, Animal, Drug Interactions, Dyskinesia, Drug-Induced, Enzyme Inhibitors, Ergolines, Female, Levodopa, Macaca fascicularis, Phosphorylation, Piperidines, Serine, Statistics as Topic, Signal Transduction, Parkinsonian Disorders, Glycogen Synthase Kinase 3, Oncogene Protein v-akt
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