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

Objective: Several findings support the concept that sensorimotor integration is disturbed in Parkinson's disease (PD) and in levodopa-induced dyskinesias. 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. Methods: Single unit activity and local field potential were recorded under urethane (1.4 g/kg, i.p) anesthesia by using quartz coated micro-electrode. Additionally, an electrocorticogram (ECoG) was acquired via a 1 mm diameter jeweller's screw, positioned on the dura mater above the MCtx ipsilateral to the 6-OHDA lesioned hemisphere. 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. [ABSTRACT FROM AUTHOR]