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dc.identifier.urihttp://hdl.handle.net/11401/77011
dc.description.sponsorshipThis work is sponsored by the Stony Brook University Graduate School in compliance with the requirements for completion of degree.en_US
dc.formatMonograph
dc.format.mediumElectronic Resourceen_US
dc.language.isoen_US
dc.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dc.typeDissertation
dcterms.abstractParkinson'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.
dcterms.available2017-09-20T16:51:39Z
dcterms.contributorEvinger, Leslie Cen_US
dcterms.contributorRobinson, Johnen_US
dcterms.contributorMohanty, Aprajitaen_US
dcterms.contributorAnderson, Brenda Jen_US
dcterms.contributorFontanini, Alfredo.en_US
dcterms.creatorKaminer, Jaime
dcterms.dateAccepted2017-09-20T16:51:39Z
dcterms.dateSubmitted2017-09-20T16:51:39Z
dcterms.descriptionDepartment of Biopsychology.en_US
dcterms.extent124 pg.en_US
dcterms.formatApplication/PDFen_US
dcterms.formatMonograph
dcterms.identifierhttp://hdl.handle.net/11401/77011
dcterms.issued2014-12-01
dcterms.languageen_US
dcterms.provenanceMade available in DSpace on 2017-09-20T16:51:39Z (GMT). No. of bitstreams: 1 Kaminer_grad.sunysb_0771E_11937.pdf: 2815845 bytes, checksum: 9eaebf7bf7d762b2fb3b1e4bccc117f7 (MD5) Previous issue date: 1en
dcterms.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dcterms.subjectBasal Ganglia, Blink, Deep Brain Stimulation, Parkinson's Disease
dcterms.subjectNeurosciences
dcterms.titleThe Role of Beta Activity in Blink Abnormalities in a Rat Model of Parkinson's Disease
dcterms.typeDissertation


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