Early-onset cortico-cortical synchronization in the hemiparkinsonian rat model.
Changes in synchronized neuronal oscillatory activity are reported in both cortex and basal ganglia of Parkinson's disease patients. The origin of these changes, in particular their relationship with the progressive nigrostriatal dopaminergic denervation, is unknown. Therefore, in the present study we studied interregional neuronal synchronization in motor cortex and basal ganglia during the development of dopaminergic degeneration induced by a unilateral infusion of 6-hydroxydopamine (6-OHDA) into the rat medial forebrain bundle. We performed serial local field potential recordings bilaterally in the motor cortex and the subthalamic nucleus of the lesioned hemisphere prior to, during, and after development of the nigrostriatal dopaminergic cell loss. We obtained signal from freely moving rats in both resting and walking conditions, and we computed local spectral power, interregional synchronization (using phase lag index), and directionality (using Granger causality). After neurotoxin injection the first change in phase lag index was an increment in cortico-cortical synchronization. We observed increased bidirectional Granger causality in the beta frequency band between cortex and subthalamic nucleus within the lesioned hemisphere. In the walking condition, the 6-OHDA lesion-induced changes in synchronization resembled that of the resting state, whereas the changes in Granger causality were less pronounced after the lesion. Considering the relatively preserved connectivity pattern of the cortex contralateral to the lesioned side and the early emergence of increased cortico-cortical synchronization during development of the 6-OHDA lesion, we suggest a putative compensatory role of cortico-cortical coupling.
Department of Anatomy and Neurosciences, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands; b.duray@vumc.nl.
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BN
Jávor-Duray
Cognitive and Systems Neuroscience, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands;
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M
Vinck
Department of Anatomy and Neurosciences, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands;
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M
van der Roest
Department of Anatomy and Neurosciences, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands;
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AB
Mulder
Department of Clinical Neurophysiology, VU University Medical Center, Amsterdam, The Netherlands; and.
C J
CJ
Stam
Department of Neurology, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands.
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HW
Berendse
Department of Anatomy and Neurosciences, VU University Medical Center, Neuroscience Campus Amsterdam, Amsterdam, The Netherlands;
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Voorn
D000818:Animals; D001479:Basal Ganglia / Q000502:physiology; D001611:Beta Rhythm; D003344:Cortical Synchronization; D008124:Locomotion; D008297:Male; D009044:Motor Cortex / Q000502:physiology*; D016627:Oxidopamine / Q000633:toxicity; D010302:Parkinson Disease, Secondary / Q000209:etiology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012146:Rest
D016627:Oxidopamine
6-OHDA; Parkinson's disease; cortex; in vivo neurophysiology; subthalamic nucleus