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

- Imbalance of excitatory and inhibitory sensorimotor cortical neuronal activity in 6-OHDA-lesioned rats
- Enhanced theta/alpha (5-12 Hz) synchronization in levodopa induced dyskinetic rats
- Shifting of high beta and gamma oscillatory activity in hemi-parkinsonian and levodopa induced dyskinetic rats.
- An increase of the vesicular GABA transporter Vgat in levodopa-induced dyskinetic rats.

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 under urethane (1.4 g/kg, i.p.) anesthesia. Further, gene expression patterns of distinct markers for inhibitory GABAergic neurons were analyzed in both cortical regions.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 putative 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.Our study shows that in a rat model of PD with dyskinesias, neuronal activity in putative interneurons was reduced, which was accompanied by high beta and gamma coherence between S1FL-Ctx and MCtx, together with changes in gene expression, indicating maladaptive neuroplasticity after long term levodopa treatment.