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dc.contributor.advisorRobert Desimone and Ed Boyden.en_US
dc.contributor.authorAcker, Leah C. (Leah Christine)en_US
dc.contributor.otherHarvard--MIT Program in Health Sciences and Technology.en_US
dc.date.accessioned2015-03-05T15:57:05Z
dc.date.available2015-03-05T15:57:05Z
dc.date.copyright2014en_US
dc.date.issued2014en_US
dc.identifier.urihttp://hdl.handle.net/1721.1/95859
dc.descriptionThesis: Ph. D., Harvard-MIT Program in Health Sciences and Technology, 2014.en_US
dc.descriptionCataloged from PDF version of thesis.en_US
dc.descriptionIncludes bibliographical references (pages 130-139).en_US
dc.description.abstractPharmacological inactivation studies have shown that the frontal eye field (FEF) is critical for executing saccades to remembered locations. FEF neurons increase their firing rate during the three epochs of the memory-guided saccade task: visual stimulus presentation, the delay interval, and motor preparation. It is unclear, though, whether FEF activity during each epoch is necessary for memory-guided saccade execution. To address this question, techniques for millisecond-precise optical inactivation of the primate brain were invented. A red-shifted halorhodopsin (Jaws) and a novel large-volume tissue illuminator were used in two rhesus macaques to inactivate part of the FEF at different times during the memory-guided saccade task. Neuronal recordings showed that the inactivated tissue volume (i.e., the volume where the firing rate of >80% of neurons decreased by >80%) spanned several cubic millimeters, which is consistent with histological findings. When the target was in the inactivated receptive field, error rates (i.e., failures to execute memory-guided saccades to the proper target location) increased in both monkeys with inactivation during either the target, delay, or motor period. This implies that FEF neuronal activity contributes to performance throughout the memory-guided saccade task.en_US
dc.description.statementofresponsibilityby Leah C. Acker.en_US
dc.format.extent139 pagesen_US
dc.language.isoengen_US
dc.publisherMassachusetts Institute of Technologyen_US
dc.rightsM.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.en_US
dc.rights.urihttp://dspace.mit.edu/handle/1721.1/7582en_US
dc.subjectHarvard--MIT Program in Health Sciences and Technology.en_US
dc.titleOptogenetic disruption of memory-drive, oculomotor behavior in the non-human primateen_US
dc.typeThesisen_US
dc.description.degreePh. D.en_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technology
dc.identifier.oclc904048676en_US


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