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dc.identifier.urihttp://hdl.handle.net/11401/76564
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.abstractThe trigeminal blink reflex is a simple circuit for investigating the neural bases of motor plasticity in mammals. Stimulating the supraorbital branch of the trigeminal nerve (SO) evokes two bursts of activity in the lid closing orbicularis oculi muscle, R1 and R2. One procedure for inducing blink plasticity is high frequency stimulation (HFS) of the SO. Presenting HFS before the R2 component (HFS-B) reduces blink amplitude for at least one hour in humans and rats. This reduction in blink amplitude is a decrease in gain because the blink evoking stimulus is the same before and after HFS-B treatment. To identify neurons in the trigeminal blink circuit that participate in this form of blink plasticity c-Fos immunohistochemistry was utilized. One group of rats underwent HFS-B treatment and a second control group received individual SO stimuli instead of HFS-B treatment. The data showed that the number of c-Fos labeled neurons in the trigeminal nucleus correlated inversely with the reduction in reflex blink gain. The cerebellum plays a major role in motor plasticity. To investigate whether the cerebellum participated in blink reflex plasticity, c-Fos labeling was measured in a cerebellar input nucleus, the inferior olive (IO) and the red nucleus, which receives an output from the cerebellum. As with the trigeminal complex, the number of c-Fos labeled cells in the IO and RN correlated inversely with the reduction in reflex blink gain. The inverse relationship between the number of c-Fos labeled cells and the suppression of trigeminal reflex blink circuit activity suggests that circuit inhibition requires activating more cells than enhancing trigeminal blink circuit activity. These data are important in considering how pathological states modulate trigeminal reflex blink circuits.
dcterms.available2017-09-20T16:50:39Z
dcterms.contributorKritzer, Maryen_US
dcterms.contributorEvinger, Leslie Cen_US
dcterms.contributorCollins, Williamen_US
dcterms.contributorFontanini, Alfredoen_US
dcterms.contributorRobinson, John.en_US
dcterms.creatorEnmore, Patricia Ronessa
dcterms.dateAccepted2017-09-20T16:50:39Z
dcterms.dateSubmitted2017-09-20T16:50:39Z
dcterms.descriptionDepartment of Neuroscienceen_US
dcterms.extent84 pg.en_US
dcterms.formatMonograph
dcterms.formatApplication/PDFen_US
dcterms.identifierhttp://hdl.handle.net/11401/76564
dcterms.issued2016-12-01
dcterms.languageen_US
dcterms.provenanceMade available in DSpace on 2017-09-20T16:50:39Z (GMT). No. of bitstreams: 1 Enmore_grad.sunysb_0771E_13211.pdf: 2862297 bytes, checksum: 6273e099fa7e77f2fee90de71a2de02c (MD5) Previous issue date: 1en
dcterms.publisherThe Graduate School, Stony Brook University: Stony Brook, NY.
dcterms.subjectNeurosciences
dcterms.titleNeuronal Activation with Gain Modification of the Trigeminal Blink Reflex
dcterms.typeDissertation


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