Session Information
Date: Tuesday, June 21, 2016
Session Title: Parkinson's disease: Pathophysiology
Session Time: 12:30pm-2:00pm
Location: Exhibit Hall located in Hall B, Level 2
Objective: To clarify the pathogenetic role of Beta band (βb) and Gamma band (γb) in 6-OHDA-treated freely-moving rats, by combining histochemical and electrophysiological investigations.
Background: Oscillatory theory may explain most of the benefits promoted by Deep Brain Stimulation in patients afflicted by Parkinson’s disease (PD). An enhanced βb neuronal activity features basal ganglia discharge during PD akinesia, as evaluated during stereotactic neurosurgery in humans as well as in disease rodent’s models; yet, it is not from fully elucidated whether higher βb participate indeed the behavioral pathogenesis or represents a mere correlative hallmark. A less explored phenomenon regards the putative contribution of the activity to PD pathophysiology.
Methods: We have monitored these frequency bands through a careful analysis, which combined both histological and electrophysiological assessments in freely moving rats, following traditional unilateral 6-OHDA lesioning; recordings were taken from unilateral globus pallidus – GP – and bilateral frontal cortex. Hence, we acquired parameters right after denervation, after 2-4-6 weeks, and after levodopa therapy (in groups exhibiting or not severe involuntary movements).
Results: It was detected a significant increase of both power and coherence of the βb (18-30 hz) activity within the first days after the toxin injection, while both power and coherence γb remained quite constant. Notably, the increase βb discharge affected also cortex contralateral to the lesion. Dopaminergic treatment influenced in opposite ways only the power of the two examined bands, reverting βb but increasing the expression of the γb; however, the latter phenomenon occurred only in those animals manifesting dyskinesia. If, on one hand, βb activity increased parallel to the emerging of PD akinesia and impaired TH-staining, on the other hand, dyskinesia correlated strongly with γb activity. Of interest, dopaminergic treatment had a negligible effect on the intercortical and cortico-pallidal coherence attesting a genuine intra-structural phenomenon underlying the clinical off-on transition.
Conclusions: We are suggesting that, albeit a normal γb exerts a physiological pro-kinetic role, an exuberant cortical γb influences the unmasking and intensity of dyskinesia. These results may support the on-going approaches utilizing TMS or aTCD in order to modulate PD complications.
To cite this abstract in AMA style:
S. Galati, V. D'Angelo, A. Salvadè, A. Kaelin, A. Stefani. An exuberant cortical γb influences the unmasking and intensity of dyskinesia in 6-OHDA-treated freely-moving rats [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/an-exuberant-cortical-b-influences-the-unmasking-and-intensity-of-dyskinesia-in-6-ohda-treated-freely-moving-rats/. Accessed December 9, 2024.« Back to 2016 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/an-exuberant-cortical-b-influences-the-unmasking-and-intensity-of-dyskinesia-in-6-ohda-treated-freely-moving-rats/