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Judith R Walters - One of the best experts on this subject based on the ideXlab platform.
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effects of l dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of parkinson s disease
Neurobiology of Disease, 2016Co-Authors: Kristin B Dupre, Ana V Cruz, Alex J Mccoy, Claire Delaville, Colin M Gerber, Katherine W Eyring, Judith R WaltersAbstract: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.
Kristin B Dupre - One of the best experts on this subject based on the ideXlab platform.
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effects of l dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of parkinson s disease
Neurobiology of Disease, 2016Co-Authors: Kristin B Dupre, Ana V Cruz, Alex J Mccoy, Claire Delaville, Colin M Gerber, Katherine W Eyring, Judith R WaltersAbstract: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.
Mark J. Millan - One of the best experts on this subject based on the ideXlab platform.
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Simultaneous quantification of Serotonin, dopamine and noradrenaline levels in single frontal cortex dialysates of freely-moving rats reveals a complex pattern of reciprocal auto- and heteroreceptor-mediated control of release
Neuroscience, 1998Co-Authors: A. Gobert, J.-m. Rivet, V Audinot, Adrian Newman-tancredi, Laetitia Cistarelli, Mark J. MillanAbstract:Abstract In the present study, a novel and exceptionally sensitive method of high-performance liquid chromatography coupled to coulometric detection, together with concentric dialysis probes, was exploited for an examination of the role of autoreceptors and heteroceptors in the modulation of dopamine, noradrenaline and Serotonin levels in single samples of the frontal cortex of freely-moving rats. The selective D 3 /D 2 receptor agonist, CGS 15855A [(±)- trans -1,3,4,4a,5,10b-hexahydro-4-propyl-2H-[1]benzopyrano[3,4-b]-pyridin-9-ol], and Antagonist, raclopride, respectively decreased (−50%) and increased (+60%) levels of dopamine without significantly modifying those of Serotonin and noradrenaline. The selective α 2 -adrenergic receptor agonist, dexmedetomidine, markedly decreased noradrenaline levels (−100%) and likewise suppressed those of Serotonin and dopamine by −55 and −45%, respectively. This effect was mimicked by the preferential α 2A -adrenergic receptor agonist, guanabenz (−100%, −60% and −50%). Furthermore, the α 2 -adrenergic receptor Antagonist, RX 821,002 [2(2-methoxy-1,4-benzodioxan-2-yl)-2-imidazoline], and the preferential α 2A -adrenergic receptor Antagonist, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole], both evoked a pronounced elevation in levels of noradrenaline (+212%, +109%) and dopamine (+73%, +85%). In contrast, the preferential α 2B/2C -adrenergic receptor Antagonist, prazosin, did not modify noradrenaline and dopamine levels. RX 821,002 and BRL 44408 did not significantly modify levels of Serotonin, whereas prazosin decreased these levels markedly (−55%), likely due to its α 1 -adrenergic receptor Antagonist properties. The selective Serotonin-1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), reduced Serotonin levels (−65%) and increased those of dopamine and noradrenaline by +100% and +175%, respectively. The selective Serotonin-1A Antagonist, WAY 100,635 [ N -{2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl}- N -(2-pyridinyl)cyclo-hexanecarboxamide], which had little affect on monoamine levels alone, abolished the influence of 8-OH-DPAT upon Serotonin and dopamine levels and significantly attenuated its influence upon noradrenaline levels. Finally, the selective Serotonin-1B agonist, GR 46611 [3-[3-(2-dimethylaminoethyl)-1H-indol-5-yl]- N -(4-methoxybenzyl)acrylamide], decreased Serotonin levels (−49%) and the Serotonin-1B Antagonist, GR 127,935 [ N -[4-methoxy- 3-(4-methylpiperazin-1-yl)phenyl]-2′-methyl-4′-(5-methyl-1,2,4-oxadiazol-3-yl)-biphenyl-4-carboxamide], which did not significantly modify Serotonin levels alone, abolished this action of GR 46611. Levels of dopamine and noradrenaline were not affected by GR 46611 or GR 127,935. In conclusion, there is a complex pattern of reciprocal autoreceptor and heteroceptor control of monoamine release in the frontal cortex. Most notably, activation of α 2 -adrenergic receptors inhibits the release of noradrenaline, dopamine and Serotonin in each case, while stimulation of Serotonin-1A receptors suppresses Serotonin, yet facilitates noradrenaline and dopamine release. In addition, dopamine D 2 /D 3 autoreceptors restrain dopamine release while (terminal-localized) Serotonin-1B receptors reduce Serotonin release. Control of Serotonin release is expressed phasically and that of noradrenaline and dopamine release tonically.
Katherine W Eyring - One of the best experts on this subject based on the ideXlab platform.
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effects of l dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of parkinson s disease
Neurobiology of Disease, 2016Co-Authors: Kristin B Dupre, Ana V Cruz, Alex J Mccoy, Claire Delaville, Colin M Gerber, Katherine W Eyring, Judith R WaltersAbstract: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.
Colin M Gerber - One of the best experts on this subject based on the ideXlab platform.
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effects of l dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of parkinson s disease
Neurobiology of Disease, 2016Co-Authors: Kristin B Dupre, Ana V Cruz, Alex J Mccoy, Claire Delaville, Colin M Gerber, Katherine W Eyring, Judith R WaltersAbstract: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.
