Journal of Alzheimers Disease & Parkinsonism
Open Access

Abstract

Experimental works on animal models of Parkinson´s Disease (PD) and clinical studies have identified changes in the
physiology of striatal neurons that occur as a result of dopamine depletion. Many of the neuronal cell types in the striatum
are affected. The medium spiny projection neurons (MSNs) that give rise to the direct and indirect pathways of the basal
ganglia, striatal interneurons such as the tonically active neurons (TANs, largely corresponding the cholinergic interneurons)
and the fast-spiking parvalbumin-containing interneurons (FSIs) whose synaptic pattern is changed drastically after dopamine
removal.These neuronal changes have consequences on the overall neuronal activity and changes in long field potentials(LFPs)
activity have been identified across the cortico-basal ganglia circuits both clinically and experimentally. Landmark features
in PD are the alterations in the brain oscillations increased beta-band activity and diminished gamma-band activity have
been described in association with this pathology and these changes may be critical to both motor and cognitive deficits that
occur in Parkinsonian patients. Dopamine loss in PD occurs first in the dorsolateral striatum (DLS) before other striatal and
extrastriatal regions are gradually affected. The DLS is implicated in the acquisition and performance of habits and procedural
behaviors and dopamine may be required for these learning and motor related functions of the DLS. I will review here my
studies in which the consequences of dopamine depletion and L-DOPA therapy on task-related striatal network activity have
been identified. Both the firing activity of the different sub-classes of striatal neurons and oscillatory field activitywere affected
in a very specific manner in an animal model of early PD during the performance and acquisition of a procedural task.
Moreover, I will address the similarities and differences in brain oscillations and a common key feature that may be behind the
next future therapeutic target in PD research.

Biography