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dc.contributor.authorGore, Joanna Leaen
dc.date2008-07-16 12:06:19.188
dc.date.accessioned2008-07-22T14:43:42Z
dc.date.available2008-07-22T14:43:42Z
dc.date.issued2008-07-22T14:43:42Z
dc.identifier.urihttp://hdl.handle.net/1974/1331
dc.descriptionThesis (Ph.D, Physiology) -- Queen's University, 2008-07-16 12:06:19.188en
dc.description.abstractAn important function of the brain is to inhibit irrelevant behaviors. This thesis examines the role of the basal ganglia in response suppression using saccadic eye movements as a model of behavior. We measured the activity of single saccade-related neurons in primate Substantia Nigra pars reticulata (SNr), a main output structure of the basal ganglia, while the context surrounding the initiation and suppression of saccades was manipulated. Inserting a temporal gap of no stimuli between the disappearance of a central visual fixation point and the appearance of a peripheral visual target leads to a reduction in saccadic reaction times (SRT); the ‘gap’ effect. SNr pause neurons decreased their activity during the gap and this decrease correlated with SRT. This finding suggests the SNr may contribute directly to producing the gap effect and that signals related to the effect are propagating through a frontal-basal ganglia circuitry to impact pre-saccade processing. Interleaving pro-saccade (look towards a visual stimulus) and anti-saccade (look away from visual stimulus) trials allowed us to investigate how neural processes change when preparing to suppress a saccade instead of making one automatically. We show that SNr neurons exhibit activity consistent with both suppression of automatic responses and facilitation of voluntary responses, during anti-saccades. These data provide direct neurophysiological evidence for a dual role of inhibitory and disinhibitory basal ganglia outputs in the flexible shaping of behavior. Parkinson’s disease (PD) is a neurodegenerative disorder that impairs motor function due to depletion of dopamine in the striatum. Using an oculomotor countermanding paradigm, we found that PD patients were unable to suppress saccades to a peripheral target, providing evidence that the SNr performs a gating function that mediates the initiation and suppression of saccades. When pathology to the circuitry occurs, inhibitory control over saccades is affected. In Conclusion, using a variety of behavioral contexts, this thesis has demonstrated that the basal ganglia, specifically the SNr, mediates the suppression and voluntary initiation of saccades, possibly via an inhibitory gating mechanism, and that this role is important for successful interaction with a dynamic environment.en
dc.format.extent1684999 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoengen
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectSaccadeen
dc.subjectBasal Gangliaen
dc.subjectParkinson's Diseaseen
dc.subjectElectrophysiologyen
dc.titleInvestigating the contribution of the basal ganglia in the selective gating of saccade initiationen
dc.typethesisen
dc.description.degreePhDen
dc.contributor.supervisorMunoz, Douglas P.en
dc.contributor.departmentPhysiologyen
dc.degree.grantorQueen's University at Kingstonen


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