Thesis (Ph.D.)--Boston University / The present research stemmed from (a) Mayer's finding that there is no generalization between contralateral sites in the visual cortex of the albino rat (when the sites were stimulated by way of implanted electrodes, one being used as a conditioned stimulus, the other as a test stimulus in order to measure the extent of generalization); (b) anatomical data on the visual cortex, e.g., Nauta and Bucher's finding of rich inter-connections among the cells of the visual cortex of the same side (in the rat), and similar findings by Sholl with regard to the cat; and (c) the work of Myers, who found (with cats) that interocular transfer always appears unless both the posterior corpus callosum and the decussating fibers of the optic chiasm are cut. If (1) generalization between the activity of different parts of the brain on intact neural inter-connections between these areas (as suggested by Myers' research) and (2) cells in the ipsilateral visual cortex of rats are richly interconnected (as Nauta and Bucher,report}, then one should expect substantial generalization from one site in the visual cortex to another on the same side [TRUNCATED].

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Human visual perception changes across the lifespan that relies on changes in synaptic plasticity in the visual cortex. Anatomical studies of the visual cortex, however, suggest human V1 develops early and remains relatively constant from childhood and on. Animal models have pin-pointed specific neurobiological mechanisms that are necessary for the development of visual plasticity and receptive field properties in the visual cortex. Very little is known, however, about how those synaptic mechanisms develop in the human visual cortex to support plasticity and perception across the lifespan. This thesis addresses this gap by providing new studies on the development of those neurobiological mechanisms in postmortem human visual cortex cases that range in age from 20 days to 79 years. The main findings from this thesis support prolonged development of plasticity mechanisms in human V1 that could be characterized in 5 stages of change across the lifespan: booting up synaptic function in infancy, high neural variability in young childhood, peaks of development in older childhood, prolonged plasticity in adulthood, and return to juvenile-like state in aging. In addition, I show a contrasting development of synaptic plasticity mechanisms in V1 and extrastriate areas that suggest higher order visual perception is processed differently. I also highlight a modernized technique for isolating synaptoneurosomes in human brain that helps quantify synaptic proteins using postmortem human tissue. Together these findings aid in the translation of neurobiological mechanisms in animal models for identifying new therapeutic targets for recovery in human visual disorders and vision loss. / Thesis / Doctor of Philosophy (PhD) / The ability to see the world constantly changes from birth to old age, and depends on the health and function of our brain. The visual cortex is the part of the brain that processes vision, and it is made up of millions of cells that connect to each other through billions of synapses. Fine-tuning those connections and networks in the brain leads to better vision. The ability for connections to be fine-tuned by experience is called plasticity, and it is necessary for developing good vision. This thesis addresses the development of plasticity in the human brain by measuring levels of proteins that are responsible for controlling plasticity and vision. My findings suggest that humans have a longer period of plasticity for developing good vision than previously thought. These findings will help identify new targets to rescue vision loss that occurs in aging or visual disorders across the lifespan.

Thesis (Ph. D.)--University of Minnesota, 1999. / Includes bibliographical references (leaves 240-248). Also available on the World Wide Web as a PDF file.

Residual vision, or blindsight, following damage to the primary visual cortex was first identified almost a century ago. However, the mechanism and pathways underlying this ability, as well as the extent of visual function, remain unclear and are a continuing source of speculation. The work presented here goes some way to try to address these questions, investigating 18 patients with V1 damage and homonymous visual field loss acquired in adulthood. Six experimental chapters explore the extent and potential for visual function after V1 damage, and apply novel neuroimaging paradigms and techniques to try to uncover the mechanisms and pathways that might be involved. A combination of psychophysics, functional and structural MRI was used to investigate responses to blind field stimulation in the dorsal and ventral streams. In addition, diffusion MRI tractography was performed and related to psychophysical performance, so that the three main pathways implicated in blindsight could be evaluated. Lastly, a small rehabilitation study was carried out to assess the effect of training in the blind hemifield, and to investigate whether there is any transfer of learning between the dorsal and ventral visual streams. The results from this work reinforce the suggestion that blindsight may be more common than was first thought, and may extend across a number of characteristics involving both visual streams. It is also suggested that visual function need not be completely unconscious, but that certain salient stimuli can elicit both non-visual and crude visual experience. The use of parametric functional imaging paradigms has enabled a number of properties of non-striate inputs to the extrastriate cortex to be revealed. Together with tractography, this points to an important role for the ipsilateral lateral geniculate nucleus in blindsight function. It is hoped that future work will build upon this, and that it may be possible to target these residual pathways in the rehabilitation of patients with V1 damage.

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Thesis (Ph. D. in Biomedical Engineering)--Vanderbilt University, Dec. 2007. / Title from title screen. Includes bibliographical references.

The overall goals of this dissertation were 1) to understand the role that neurons in primate primary visual cortex (V1) play in the detection of small visual stimuli, and 2) to understand the quantitative relationship between the responses of individual neurons and neural population responses in V1. These goals were addressed in experiments with awake, behaving macaque monkeys using electrophysiological and imaging techniques. Initially, I employed ideal observer models to assess V1 neural detection sensitivity in a reaction-time visual detection task and found it to be comparable to the monkey's detection sensitivity. Using the same detection task, I found weak, but significant, correlations between V1 neural activity and the trial-by-trial behavior of monkeys (choice and reaction time). The conclusion of these studies is that the monkey's behavior in the detection task was likely mediated by large neural populations. Voltage-sensitive dye imaging (VSDI) is a powerful imaging technique that is well suited for assessing the link between the activity of large neural populations and behavior. VSDI measures changes in membrane potential over a cortical area of 1-2 cm² with high spatial and temporal resolutions. Using position tuning experiments with VSDI and electrophysiology, I described the relatively unknown quantitative relationships between spiking activity, the local field potential, and VSDI. These relationships were well captured by non-linear transfer functions. Lastly, these experiments also revealed important new findings about the representation of visual space by populations of neurons in V1. In particular, we resolved a long standing debate regarding the size of the cortical point image (CPI), the area of cortex activated by a single point stimulus. We found that the CPI is constant across eccentricity in parafoveal V1, suggesting that each point in space activates an approximately equivalent amount of cortical tissue. In conclusion, the results and analyses described in this dissertation contribute to our understanding of the role that neural populations in V1 play in mediating visual detection, reveal important properties of the representation of visual space by populations of neurons in V1, and provide the first analysis of the quantitative relationship between VSDI and electrophysiological signals. / text