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 |
Contributor organization: | Regenerative pharmacology group Division of Pharmacology and Pharmacotherapy Clinical Pharmacy Group Faculty of Pharmacy Laboratory of Neurotherapeutics Biosciences Drug Research Program Physiology and Neuroscience (-2020) Outi Salminen / Principal Investigator Divisions of Faculty of Pharmacy DAPHNE - Developing Assessment Practices in Higher Education Teachers' Academy |
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 |
Peer reviewed: | Yes |
Rights: | cc_by_nc |
Usage restriction: | openAccess |
Self-archived version: | publishedVersion |
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