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68th Annual Meeting of the German Society of Neurosurgery (DGNC)
7th Joint Meeting with the British Neurosurgical Society (SBNS)

German Society of Neurosurgery (DGNC)

14 - 17 May 2017, Magdeburg

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Altered somatosensory cortex neuronal activity in a rat model of Parkinson's disease and levodopa-induced dyskinesias

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  • Mesbah Alam - Department of Neurosurgery, Hannover Medical School, Hannover, Deutschland
  • Regina Rumpel - Institute of Neuroanatomy, Hannover Medical School, Hannover, Deutschland
  • Xingxing Jin - Department of Neurosurgery, Hannover Medical School, Hannover, Deutschland
  • Christof von Wrangel - Department of Neurosurgery, Charité Universitätsmedizin Berlin, Berlin, Deutschland
  • Sarah Tschirner - Institute of Neuroanatomy, Hannover Medical School, Hannover, Deutschland
  • Joachim Krauss - Department of Neurosurgery, Hannover Medical School, Hannover, Deutschland
  • Claudia Grothe - Institute of Neuroanatomy, Hannover Medical School, Hannover, Deutschland
  • Andreas Ratzka - Institute of Neuroanatomy, Hannover Medical School, Hannover, Deutschland
  • Kerstin Schwabe - Department of Neurosurgery, Hannover Medical School, Hannover, Deutschland

Deutsche Gesellschaft für Neurochirurgie. Society of British Neurological Surgeons. 68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS). Magdeburg, 14.-17.05.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocP 082

doi: 10.3205/17dgnc645, urn:nbn:de:0183-17dgnc6456

Published: June 9, 2017

© 2017 Alam et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: Several findings support the concept that sensorimotor integration is disturbed in Parkinson`s disease (PD) and in levodopa-induced dyskinesias. In PD altered neuronal connectivity activity occurs between subcortical basal ganglia (BG) and cortical circuits, where impaired somatosensory signals may influence desired motor programs.

Methods: In this study, we explored the neuronal firing activity of excitatory pyramidal cells and inhibitory interneurons in the forelimb region of the primary somatosensory cortex (S1FL-Ctx), along with its interaction with oscillatory activity of the primary motor cortex (MCtx) in 6-hydroxydopamine lesioned hemiparkinsonian (HP) and levodopa-primed dyskinetic (HP-LID) rats as compared to controls. Further, gene expression patterns of distinct markers for inhibitory GABAergic neurons were analyzed in both cortical regions.

Results: While firing frequency and burst activity of S1FL-Ctx inhibitory interneurons were reduced in HP and HP-LID rats, measures of irregularity were enhanced in pyramidal cells. Further, enhanced coherence of distinct frequency bands of the theta/alpha, high-beta, and gamma frequency, together with enhanced synchronization of pyramidal cells and interneurons with MCtx oscillatory activity were observed. While GABA level was similar, gene expression levels of interneuron and GABAergic markers in S1FL-Ctx and MCtx of HP-LID rats differed to some extent.

Conclusion: Our study shows both electrophysiological alterations and changes in gene expression in the sensorimotor cortices in a rat model of PD, which differ depending on the functional state after dopamine depletion and treatment indicating maladaptive neuroplasticity.