Tass P.A.,Julich Research Center |
Tass P.A.,University of Cologne |
Qin L.,China Academy of Medical science |
Hauptmann C.,Julich Research Center |
And 12 more authors.
Annals of Neurology | Year: 2012
Coordinated reset neuromodulation consists of the application of consecutive brief high-frequency pulse trains through the different contacts of the stimulation electrode. In theoretical studies, by achieving unlearning of abnormal connectivity between neurons, coordinated reset neuromodulation reduces pathological synchronization, a hallmark feature of Parkinson's disease pathophysiology. Here we show that coordinated reset neuromodulation of the subthalamic nucleus has both acute and sustained long-lasting aftereffects on motor function in parkinsonian nonhuman primates. Long-lasting aftereffects were not observed with classical deep brain stimulation. These observations encourage further development of coordinated reset neuromodulation for treating motor symptoms in Parkinson disease patients. Copyright © 2012 American Neurological Association. Source
Santini E.,Karolinska Institutet |
Sgambato-Faure V.,French Institute of Health and Medical Research |
Sgambato-Faure V.,University of Lyon |
Li Q.,University of Bordeaux Segalen |
And 6 more authors.
PLoS ONE | Year: 2010
Background: In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Rasextracellular signal-regulated kinase (ERK) signalling pathways. However, very little is known, in non-human primates, about the regulation of these signalling cascades and their association with the induction, manifestation and/or maintenance of dyskinesia. Methodology/Results: We here studied, in the gold-standard non-human primate model of Parkinson's disease, the changes in PKA-dependent phosphorylation of DARPP-32 and GluR1 AMPA receptor, as well as in ERK and ribosomal protein S6 (S6) phosphorylation, associated to acute and chronic administration of L-DOPA. Increased phosphorylation of DARPP-32 and GluR1 was observed in both L-DOPA first-ever exposed and chronically-treated dyskinetic parkinsonian monkeys. In contrast, phosphorylation of ERK and S6 was enhanced preferentially after acute L-DOPA administration and decreased during the course of chronic treatment. Conclusion: Dysregulation of cAMP signalling is maintained during the course of chronic L-DOPA administration, while abnormal ERK signalling peaks during the initial phase of L-DOPA treatment and decreases following prolonged exposure. While cAMP signalling enhancement is associated with dyskinesia, abnormal ERK signalling is associated with priming. © 2010 Santini et al. Source
Yin M.,Brown University |
Borton D.A.,Brown University |
Borton D.A.,Ecole Polytechnique Federale de Lausanne |
Komar J.,Brown University |
And 15 more authors.
Neuron | Year: 2014
Brain recordings in large animal models and humans typically rely on a tethered connection, which has restricted the spectrum of accessible experimental and clinical applications. To overcome this limitation, we have engineered a compact, lightweight, high data rate wireless neurosensor capable of recording the full spectrum of electrophysiological signals fromthe cortex of mobile subjects. The wireless communication system exploits a spatially distributed network of synchronized receivers that is scalable to hundreds of channels and vast environments. To demonstrate the versatility of our wireless neurosensor, we monitored cortical neuron populations in freely behaving nonhuman primates during natural locomotion and sleep-wake transitions in ecologically equivalent settings. The interface is electrically safe and compatible with the majority of existing neural probes, which may support previously inaccessible experimental and clinical research. © 2014 Elsevier Inc. Source
Porras G.,Institut Universitaire de France |
Porras G.,French National Center for Scientific Research |
Li Q.,China Academy of Medical science |
Bezard E.,Institut Universitaire de France |
And 2 more authors.
Cold Spring Harbor Perspectives in Medicine | Year: 2012
The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) primate models of Parkinson's disease (PD) reproduce most, although not all, of the clinical and pathological hallmarks of PD. The present contribution presents the possibilities offered by the MPTP monkey models of PD to readers with minimal knowledge of PD, emphasizing the diversity of species, route and regimen of administration, symptoms and pathological features. Readers would eventually find out that there is not a single MPTP monkey model of PD but instead MPTP monkey models of PD, each addressing a specific experimental need. © 2012 Cold Spring Harbor Laboratory Press; all rights reserved. Source
Fox S.H.,University of Western Ontario |
Fox S.H.,University of Toronto |
Johnston T.H.,University of Western Ontario |
Li Q.,China Academy of Medical science |
And 4 more authors.
Movement Disorders | Year: 2012
Levodopa-induced dyskinesia (LID) is a major limitation of long-term management of Parkinson's disease. The roadblocks that have hindered the development of new treatments for levodopa-induced dyskinesia were discussed at a meeting organized by the Michael J. Fox Foundation for Parkinson's research (New York, NY, March 2011). Among these, the lack of consensus methodology and clinical applicability for eliciting and rating LID in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys was highlighted as a particular concern. Here we present an update on the practical use of rating scales for evaluating LID in MPTP-lesioned primate models of PD, with a focus on macaques, and present specifics on the Non-Human Primate Dyskinesia Rating Scale. © 2012 Movement Disorder Society. Source