Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease
| Autor: | Colin M. Gerber, Claire Delaville, Judith R. Walters, Ana V. Cruz, Alex J. McCoy, Kristin B. Dupre, Katherine W. Eyring |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Agonist Dyskinesia Drug-Induced Levodopa Quinpirole medicine.drug_class Dopamine Abnormal involuntary movements Motor Activity Article lcsh:RC321-571 Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Parkinsonian Disorders Dopamine receptor D2 L-dopa Gamma Rhythm medicine Animals Gamma Oxidopamine lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Neurons 8-Hydroxy-2-(di-n-propylamino)tetralin Dyskinesia Chemistry Motor Cortex Beta Benzazepines Abnormal involuntary movement Rats Serotonin Receptor Agonists nervous system diseases Disease Models Animal 030104 developmental biology Neurology Dopamine Agonists medicine.symptom Neuroscience 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Neurobiology of Disease, Vol 86, Iss, Pp 1-15 (2016) |
| ISSN: | 0969-9961 |
| DOI: | 10.1016/j.nbd.2015.11.009 |
| Popis: | Prolonged L-dopa treatment in Parkinson's disease (PD) often leads to the expression of abnormal involuntary movements known as L-dopa-induced dyskinesia. Recently, dramatic 80 Hz oscillatory local field potential (LFP) activity within the primary motor cortex has been linked to dyskinetic symptoms in a rodent model of PD and attributed to stimulation of cortical dopamine D1 receptors. To characterize the relationship between high gamma (70–110 Hz) cortical activity and the development of L-dopa-induced dyskinesia, cortical LFP and spike signals were recorded in hemiparkinsonian rats treated with L-dopa for 7 days, and dyskinesia was quantified using the abnormal involuntary movements (AIMs) scale. The relationship between high gamma and dyskinesia was further probed by assessment of the effects of pharmacological agents known to induce or modulate dyskinesia expression. Findings demonstrate that AIMs and high gamma LFP power increase between days 1 and 7 of L-dopa priming. Notably, high beta (25–35 Hz) power associated with parkinsonian bradykinesia decreased as AIMs and high gamma LFP power increased during priming. After priming, rats were treated with the D1 agonist SKF81297 and the D2 agonist quinpirole. Both dopamine agonists independently induced AIMs and high gamma cortical activity that were similar to that induced by L-dopa, showing that this LFP activity is neither D1 nor D2 receptor specific. The serotonin 1A receptor agonist 8-OH-DPAT reduced L-dopa- and DA agonist-induced AIMs and high gamma power to varying degrees, while the serotonin 1A antagonist WAY100635 reversed these effects. Unexpectedly, as cortical high gamma power increased, phase locking of cortical pyramidal spiking to high gamma oscillations decreased, raising questions regarding the neural substrate(s) responsible for high gamma generation and the functional correlation between high gamma and dyskinesia. |
| Databáze: | OpenAIRE |
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