Dyskinesia and brain-derived neurotrophic factor levels after long-term levodopa and nicotinic receptor agonist treatments in female mice with near-total unilateral dopaminergic denervation

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Leino , S , Kohtala , S , Rantamäki , T , Koski , S K , Rannanpää , S & Salminen , O 2018 , ' Dyskinesia and brain-derived neurotrophic factor levels after long-term levodopa and nicotinic receptor agonist treatments in female mice with near-total unilateral dopaminergic denervation ' , BMC Neuroscience , vol. 19 , no. 1 , 77 . https://doi.org/10.1186/s12868-018-0478-0

Title: Dyskinesia and brain-derived neurotrophic factor levels after long-term levodopa and nicotinic receptor agonist treatments in female mice with near-total unilateral dopaminergic denervation
Author: Leino, Sakari; Kohtala, Samuel; Rantamäki, Tomi; Koski, Sini K.; Rannanpää, Saara; Salminen, Outi
Other contributor: University of Helsinki, Regenerative pharmacology group
University of Helsinki, Laboratory of Neurotherapeutics
University of Helsinki, Drug Research Program
University of Helsinki, Regenerative pharmacology group
University of Helsinki, Regenerative pharmacology group
University of Helsinki, Regenerative pharmacology group











Date: 2018-11-29
Language: eng
Number of pages: 10
Belongs to series: BMC Neuroscience
ISSN: 1471-2202
DOI: https://doi.org/10.1186/s12868-018-0478-0
URI: http://hdl.handle.net/10138/276973
Abstract: BackgroundThe treatment of Parkinson's disease is often complicated by levodopa-induced dyskinesia (LID). Nicotinic acetylcholine receptor agonists can alleviate LID in animal models but may be less effective in conditions of severe dopaminergic denervation. While the mechanisms of LID remain incompletely understood, elevated corticostriatal levels of the brain-derived neurotrophic factor (BDNF) have been suggested to play a role. Here, female mice with near-total unilateral 6-hydroxydopamine-induced nigrostriatal lesions were chronically treated with levodopa, and the effects of the 7 nicotinic receptor partial agonist AZD0328 and nicotine on LID were assessed. At the end of the experiment, BDNF protein levels in the prefrontal cortex and striatum were measured.ResultsFive-day treatments with three escalating doses of AZD0328 and a 10-week treatment with nicotine failed to alleviate LID. BDNF levels in the lesioned striatum correlated positively with LID severity, but no evidence was found for a levodopa-induced elevation of corticostriatal BDNF in the lesioned hemisphere. The nicotine treatment decreased BDNF levels in the prefrontal cortex but had no effect on striatal BDNF.ConclusionsThe findings suggest that treatment of LID with nicotinic agonists may lose its effectiveness as the disease progresses, represent further evidence for a role for BDNF in LID, and expand previous knowledge on the effects of long-term nicotine treatment on BDNF.
Subject: AQW051
Alpha7 nicotinic receptors
BDNF
DOPA-INDUCED DYSKINESIAS
EXPRESSION
IMPROVEMENT
INCREASES
Levodopa-induced dyskinesia
MODEL
MOTOR
Nicotine
PARKINSONS-DISEASE
Parkinson's disease
RATS
SYNAPTIC PLASTICITY
3112 Neurosciences
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