Abstract
In this review, we discuss first an example of one of the symptoms of PD, freezing of gait (FOG), then we will turn to the use of deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) to treat PD, and the original studies that led to identification of the PPN as one source of locomotor control and why stimulation frequency is critical, and then describe the intrinsic properties of PPN neurons that require beta/gamma stimulation in order to fully activate all types of PPN neurons. Finally, we will describe recent findings on the proteomic and molecular consequences of gamma band activity in PPN neurons, with emphasis on the potential neuroepigenetic sequelae. These considerations will provide essential information for the appropriate refining and testing of PPN DBS as a potential therapy for PD, as well as alternative options.
Highlights
Deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) has been used for the treatment of Parkinson’s disease (PD) with beneficial effects on a number of functions, including decreasing freezing of gait (FOG), decreasing falls, and lessening balance problems
In this review, we discuss first an example of one of the symptoms of PD, freezing of gait (FOG), we will turn to the use of deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) to treat PD, and the original studies that led to identification of the PPN as one source of locomotor control and why stimulation frequency is critical, and describe the intrinsic properties of PPN neurons that require beta/gamma stimulation in order to fully activate all types of PPN neurons
We will discuss first an example of one of the symptoms of PD, FOG, we will turn to the original studies that led to identification of the PPN as one source of locomotor control and why stimulation frequency is critical, and describe the intrinsic properties of PPN neurons that require beta/gamma stimulation in order to optimally activate these neurons
Summary
Deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) has been used for the treatment of Parkinson’s disease (PD) with beneficial effects on a number of functions, including decreasing freezing of gait (FOG), decreasing falls, and lessening balance problems. The use of PPN DBS arose from our studies on animals using PPN stimulation to drive locomotion on a treadmill [1,2], and was later proposed for modulating gait in PD [3]. We will describe recent findings on the proteomic and molecular consequences of gamma band activity in PPN neurons, with emphasis on the potential neuroepigenetic sequelae. These considerations will provide essential information for the appropriate refining and testing of PPN DBS as a potential therapy for PD, as well as alternative options
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