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Alterations in functional cortical hierarchy in hemiparkinsonian rats

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Vinck,  Martin       
Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, Max Planck Society;
Vinck Lab, Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, Max Planck Society;

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Citation

Jávor-Duray, B. N., Vinck, M., van der Roest, M., Bezard, E., Berendse, H. W., Boraud, T., et al. (2017). Alterations in functional cortical hierarchy in hemiparkinsonian rats. Journal of Neuroscience, 37(32), 7669-7681. doi:10.1523/JNEUROSCI.3257-16.2017.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002E-7E43-4
Abstract
Parkinson's disease and experimentally induced hemiparkinsonism are characterized by increased beta-synchronization between cortical and subcortical areas. This change in beta-connectivity might reflect either a symmetric increase in interareal influences or asymmetric changes in directed influences among brain areas. We assessed patterns of functional and directed connectivity within and between striatum and six cortical sites in each hemisphere of the hemiparkinsonian rat model. Local field potentials were recorded in resting and walking states, before and after unilateral 6-hydroxydopamine lesion. The hemiparkinsonian state was characterized by increased oscillatory activity in the 20-40 Hz range in resting and walking states, and increased interhemispheric coupling (phase lag index) that was more widespread at rest than during walking. Spectral Granger-causality analysis revealed that the change in symmetric functional connectivity comprised profound reorganization of hierarchical organization and directed influence patterns. First, in the lesioned hemisphere, the more anterior, non-primary motor areas located at the top of the cortical hierarchy (i.e. receiving many directed influences) tended to increase their directed influence onto the posterior primary motor and somatosensory areas. This enhanced influence of "higher" areas may be related to the loss of motor control due to the 6-OHDA lesion. Second, the drive from the non-lesioned towards the lesioned hemisphere (in particular to striatum) increased, most prominently during walking. The nature of these adaptations