Type
Text
Type
Dissertation
Advisor
Evinger, Leslie C | Robinson, John | Mohanty, Aprajita | Anderson, Brenda J | Fontanini, Alfredo.
Date
2014-12-01
Keywords
Basal Ganglia, Blink, Deep Brain Stimulation, Parkinson's Disease | Neurosciences
Department
Department of Biopsychology.
Language
en_US
Source
This work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.
Identifier
http://hdl.handle.net/11401/77011
Publisher
The Graduate School, Stony Brook University: Stony Brook, NY.
Format
application/pdf
Abstract
Parkinson's disease (PD) is a devastating neurodegenerative disease that causes difficulty initiating voluntary movements among other symptoms. Electrophysiological work highlights the presence of exaggerated synchronized beta band (10-30 Hz) oscillations throughout the cortico-basal ganglia network in PD. Although a causal role of beta oscillations in PD symptoms has not been established, many hypothesize that beta activity is " antikinetic" and the source of Parkinsonian motor symptoms. This relationship remains unclear because the strength of beta oscillations changes dynamically with cues that initiate movement and because the voluntary motor symptoms of PD are often not present in animal models of PD. Therefore, studying an involuntary movement shared by all mammals is critical to understanding the role of beta oscillations in creating Parkinsonian symptoms. The blink system provides this opportunity as dopamine depletion induces identical symptoms in PD patients and the 6-hydroxydopamine (6-OHDA) rat model of PD. My investigations utilized the blink system to examine the role of beta oscillations in Parkinsonian motor symptoms. My first study examined the effect of dopamine on spontaneous blinking in rats. Dopamine depletion decreased the spontaneous blink rate as occurs in PD patients and reduced the regularity of spontaneous blinking. Disrupting beta oscillations with 130 Hz Subthalamic Nucleus Deep Brain Stimulation (STN DBS) did not attenuate these symptoms. Second, I examined the role of beta oscillations in PD blink reflex abnormalities, impaired blink plasticity and increased trigeminal reflex blink excitability. Disrupting beta oscillations with 130 Hz STN DBS restored normal plasticity and attenuated increased blink reflex excitability displayed by 6-OHDA lesioned rats. In the third study, I directly tested the role of beta oscillations in blink reflex abnormalities in PD by determining whether beta (16 Hz) stimulation was sufficient to induce Parkinsonian-like abnormalities in normal rats. Only 16 Hz STN DBS impaired reflex blink plasticity and produced reflex blink hyperexcitability in normal rats. The role of beta oscillations in blink reflex abnormalities but not spontaneous blink reduction (Study 1), suggests separate circuits for basal ganglia modulation of these behaviors. Overall, these data provide strong support for the importance of beta oscillations in the generation of Parkinsonian symptoms. | 124 pages
Recommended Citation
Kaminer, Jaime, "The Role of Beta Activity in Blink Abnormalities in a Rat Model of Parkinson's Disease" (2014). Stony Brook Theses and Dissertations Collection, 2006-2020 (closed to submissions). 2873.
https://commons.library.stonybrook.edu/stony-brook-theses-and-dissertations-collection/2873