ArticlePloS one2011
The locus coeruleus is directly implicated in L-DOPA-induced dyskinesia in parkinsonian rats: an electrophysiological and behavioural study.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Locus coeruleus α-synuclein overexpression induces prodromal Parkinsonian features in mice.NPJ Parkinson's disease · 2026Article
- Diversity of ancestral brainstem noradrenergic neurons across species and multiple biological factors.bioRxiv : the preprint server for biology · 2024Article
- The chronic use of serotonin norepinephrine reuptake inhibitors facilitates dyskinesia priming in early Parkinson's disease.Journal of neurology · 2024Article
- Grid cells: the missing link in understanding Parkinson's disease?Frontiers in neuroscience · 2024Article
- Levodopa-Induced Dyskinesias in Parkinson's Disease: An Overview on Pathophysiology, Clinical Manifestations, Therapy Management Strategies and Future Directions.Journal of clinical medicine · 2023Review
- Vagus nerve stimulation parameters evoke differential neuronal responses in the locus coeruleus.Physiological reports · 2023Article
- The effect of 5-HTBritish journal of pharmacology · 2021Article
- Circuit Mechanisms of L-DOPA-Induced Dyskinesia (LID).Frontiers in neuroscience · 2021Review
- 6-Hydroxydopamine lesion and levodopa treatment modify the effect of buspirone in the substantia nigra pars reticulata.British journal of pharmacology · 2020Article
- Changes in Day/Night Activity in the 6-OHDA-Induced Experimental Model of Parkinson's Disease: Exploring Prodromal Biomarkers.Frontiers in neuroscience · 2020Article
- The Noradrenergic System in Parkinson's Disease.Frontiers in pharmacology · 2020Review
- Impaired Phasic Discharge of Locus Coeruleus Neurons Based on Persistent High Tonic Discharge-A New Hypothesis With Potential Implications for Neurodegenerative Diseases.Frontiers in neurology · 2020Article
- L-DOPA in Parkinson's Disease: Looking at the "False" Neurotransmitters and Their Meaning.International journal of molecular sciences · 2019Review
- Long Road to Ruin: Noradrenergic Dysfunction in Neurodegenerative Disease.Trends in neurosciences · 2018Review
- The acute and long-term L-DOPA effects are independent from changes in the activity of dorsal raphe serotonergic neurons in 6-OHDA lesioned rats.British journal of pharmacology · 2016Article
- Modulation of L-DOPA's antiparkinsonian and dyskinetic effects by α2-noradrenergic receptors within the locus coeruleus.Neuropharmacology · 2015Article
- Effects of the beta-adrenergic receptor antagonist Propranolol on dyskinesia and L-DOPA-induced striatal DA efflux in the hemi-parkinsonian rat.Journal of neurochemistry · 2015Article
- Effects of noradrenergic denervation by anti-DBH-saporin on behavioral responsivity to L-DOPA in the hemi-parkinsonian rat.Behavioural brain research · 2014Article
- Modulation of the subthalamic nucleus activity by serotonergic agents and fluoxetine administration.Psychopharmacology · 2014Article
- Presynaptic Mechanisms of l-DOPA-Induced Dyskinesia: The Findings, the Debate, and the Therapeutic Implications.Frontiers in neurology · 2014Review
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4 authors.
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Abstract
Despite being the most effective treatment for Parkinson's disease, L-DOPA causes a development of dyskinetic movements in the majority of treated patients. L-DOPA-induced dyskinesia is attributed to a dysregulated dopamine transmission within the basal ganglia, but serotonergic and noradrenergic systems are believed to play an important modulatory role. In this study, we have addressed the role of the locus coeruleus nucleus (LC) in a rat model of L-DOPA-induced dyskinesia. Single-unit extracellular recordings in vivo and behavioural and immunohistochemical approaches were applied in rats rendered dyskinetic by the destruction of the nigrostriatal dopamine neurons followed by chronic treatment with L-DOPA. The results showed that L-DOPA treatment reversed the change induced by 6-hydroxydopamine lesions on LC neuronal activity. The severity of the abnormal involuntary movements induced by L-DOPA correlated with the basal firing parameters of LC neuronal activity. Systemic administration of the LC-selective noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine did not modify axial, limb, and orolingual dyskinesia, whereas chemical destruction of the LC with ibotenic acid significantly increased the abnormal involuntary movement scores. These results are the first to demonstrate altered LC neuronal activity in 6-OHDA lesioned rats treated with L-DOPA, and indicate that an intact noradrenergic system may limit the severity of this movement disorder.
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