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Thesis (Ph. D.)--University of Chicago, Committee on Neurobiology, March 1999. / Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--Drexel University, 2006. / Includes abstract and vita. Includes bibliographical references (leaves 127-162).

No description available.

Master of Science in Medicine / Saccadic and vestibular-evoked eye movements are similar in that their three-dimensional kinematic properties show eye position-dependence. When the line of sight is directed towards an eccentric target, the eye velocity axis tilts in a manner that depends on the instantaneous position of the eye in the head, with the magnitude of tilt also depending on whether the eye movement is saccadic or vestibular-evoked. The mechanism responsible for producing eye velocity axis tilting phenomena is not well understood. Some authorities have suggested that muscle pulleys in the orbit are critical for implementing eye velocity axis tilting, while others have suggested that the cerebellum plays an important role. In the current study, three-dimensional eye and head rotation data were acquired, using the magnetic search coil technique, to confirm the presence of eye position-dependent eye velocity axis tilting during saccadic eye movements. Both normal humans and humans with cerebellar atrophy were studied. While the humans with cerebellar atrophy were noted to have abnormalities in the two-dimensional metrics and consistency of their saccadic eye movements, the eye position-dependent eye velocity axis tilts were similar to those observed in the normal subjects. A mathematical model of the human saccadic and vestibular systems was utilized to investigate the means by which these eye position-dependent properties may arise for both types of eye movement. The predictions of the saccadic model were compared with the saccadic data obtained in the current study, while the predictions of the vestibular model were compared with vestibular-evoked eye movement data obtained in a previous study. The results from the model simulations suggest that the muscle pulleys are responsible for bringing about eye position-dependent eye velocity axis tilting for both saccadic and vestibular-evoked eye movements, and that these phenomena are not centrally programmed.

The vestibulo-ocular reflex (VOR) is a simple reflex that stabilizes gaze by moving the eyes in the opposite direction to the head. The gain of the VOR (ratio of head to eye velocity) can be increased or decreased during motor learning. It is thought that the memory for learned changes in the VOR gain is initially encoded within the cerebellar flocculus. Furthermore, these learned gain changes can be disrupted or consolidated into a long-term memory. In this thesis we describe novel results that show that consolidation of the VOR can take place rapidly, within 1 hour after learning has stopped. Furthermore, we demonstrated that unlike learning, which has been shown to have frequency selectivity, disruption and rapid consolidation generalize across the range of frequencies. We suggest that disruption and rapid consolidation in the VOR are local mechanisms within the cerebellar cortex, and do not require new learning. This thesis also provides additional evidence for the idea that learned gain increases and decreases are the result of separate mechanisms, most likely long-term depression and potentiation respectively, at the parallel fibre-Purkinje cell synapses. We demonstrate that learned gain increases, but not decreases, require the activation of type 1 metabotropic glutamate receptors (mGluR1) and B type γ-aminobutyric acid (GABAB) receptors. Blocking one or both of these receptors with an antagonist inverts gain-up learning, while the agonist augments gain-up learning. Furthermore, we provide novel evidence that these receptors are co-activated during gain-up learning.

The vestibulo-ocular reflex (VOR) is a simple reflex that stabilizes gaze by moving the eyes in the opposite direction to the head. The gain of the VOR (ratio of head to eye velocity) can be increased or decreased during motor learning. It is thought that the memory for learned changes in the VOR gain is initially encoded within the cerebellar flocculus. Furthermore, these learned gain changes can be disrupted or consolidated into a long-term memory. In this thesis we describe novel results that show that consolidation of the VOR can take place rapidly, within 1 hour after learning has stopped. Furthermore, we demonstrated that unlike learning, which has been shown to have frequency selectivity, disruption and rapid consolidation generalize across the range of frequencies. We suggest that disruption and rapid consolidation in the VOR are local mechanisms within the cerebellar cortex, and do not require new learning. This thesis also provides additional evidence for the idea that learned gain increases and decreases are the result of separate mechanisms, most likely long-term depression and potentiation respectively, at the parallel fibre-Purkinje cell synapses. We demonstrate that learned gain increases, but not decreases, require the activation of type 1 metabotropic glutamate receptors (mGluR1) and B type γ-aminobutyric acid (GABAB) receptors. Blocking one or both of these receptors with an antagonist inverts gain-up learning, while the agonist augments gain-up learning. Furthermore, we provide novel evidence that these receptors are co-activated during gain-up learning.

Master of Science in Medicine / Saccadic and vestibular-evoked eye movements are similar in that their three-dimensional kinematic properties show eye position-dependence. When the line of sight is directed towards an eccentric target, the eye velocity axis tilts in a manner that depends on the instantaneous position of the eye in the head, with the magnitude of tilt also depending on whether the eye movement is saccadic or vestibular-evoked. The mechanism responsible for producing eye velocity axis tilting phenomena is not well understood. Some authorities have suggested that muscle pulleys in the orbit are critical for implementing eye velocity axis tilting, while others have suggested that the cerebellum plays an important role. In the current study, three-dimensional eye and head rotation data were acquired, using the magnetic search coil technique, to confirm the presence of eye position-dependent eye velocity axis tilting during saccadic eye movements. Both normal humans and humans with cerebellar atrophy were studied. While the humans with cerebellar atrophy were noted to have abnormalities in the two-dimensional metrics and consistency of their saccadic eye movements, the eye position-dependent eye velocity axis tilts were similar to those observed in the normal subjects. A mathematical model of the human saccadic and vestibular systems was utilized to investigate the means by which these eye position-dependent properties may arise for both types of eye movement. The predictions of the saccadic model were compared with the saccadic data obtained in the current study, while the predictions of the vestibular model were compared with vestibular-evoked eye movement data obtained in a previous study. The results from the model simulations suggest that the muscle pulleys are responsible for bringing about eye position-dependent eye velocity axis tilting for both saccadic and vestibular-evoked eye movements, and that these phenomena are not centrally programmed.

Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (leaves [268]-281).

In recent experiments involving acceleration stimuli, researchers instructed subjects to focus on a visual target while measuring the vestibulo-ocular reflex (VOR) in one eye. These experiments showed conclusively that the VOR is influenced by target distance. We, on the other hand, were interested in investigating the VOR of subjects accelerated in complete darkness. Specifically, we wished to determine the subject's vergence point, which cannot be accomplished using data obtained from only one eye. Hence, a binocular eye-tracking system that works in the dark was required. In the experiment described in this thesis, the subject was rotated in the dark on NAMRL's Coriolis Acceleration Platform. The position of each pupil center was tracked and recorded by two helmet-mounted infrared cameras connected to a computer-controlled data acquisition system. The position data were used to calculate the angles through which the eyes rotated, and then trigonometric principles were applied to construct the line of sight for each eye for any moment in time; the intersection of these two lines is the vergence point. With the NAMRL binocular eye-tracking system, an accelerating subject's vergence point can accurately be determined if it is less than 1. 5 meters away. The vergence data obtained from this experiment suggest that vergence distance does not exclusively drive the VOR in the dark. / Master of Science