Type

Text

Type

Dissertation

Advisor

Evinger, Leslie C | Kritzer, Mary | Collins, William | Fontanini, Alfredo | Robinson, John.

Date

2016-12-01

Keywords

Neurosciences

Department

Department of Neuroscience

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/11401/76564

Publisher

The Graduate School, Stony Brook University: Stony Brook, NY.

Format

application/pdf

Abstract

The 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. | 84 pages

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