ASU Electronic Theses and Dissertations
This collection includes most of the ASU Theses and Dissertations from 2011 to present. ASU Theses and Dissertations are available in downloadable PDF format; however, a small percentage of items are under embargo. Information about the dissertations/theses includes degree information, committee members, an abstract, supporting data or media.
In addition to the electronic theses found in the ASU Digital Repository, ASU Theses and Dissertations can be found in the ASU Library Catalog.
Dissertations and Theses granted by Arizona State University are archived and made available through a joint effort of the ASU Graduate College and the ASU Libraries. For more information or questions about this collection contact or visit the Digital Repository ETD Library Guide or contact the ASU Graduate College at gradformat@asu.edu.
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- All Subjects: Neurosciences
The first two experiments set out to correlate microsaccade production with the visibility of foveal and peripheral targets of varied spatial frequencies, during attempted fixation. The results indicate that microsaccades restore the visibility of both peripheral targets and targets presented entirely within the fovea, as a function of their spatial frequency characteristics.
The last two experiments set out to determine the role of microsaccades and drifts on the correction of gaze-position errors due to blinks in human and non-human primates, and to characterize microsaccades forming square-wave jerks (SWJs) in non-human primates. The results showed that microsaccades, but not drifts, correct gaze-position errors due to blinks, and that SWJ production and dynamic properties are equivalent in human and non-human primates.
These combined findings suggest that microsaccades, like saccades, serve multiple and non-exclusive functional roles in vision and oculomotor control, as opposed to having a single specialized function.
First, a spatially collapsed model is used to develop voltage gated ion channels to study the excitability of the model neuron. Changing the channel densities reproduces different in situ observed firing patterns and induces a switch from resonator to integrator properties. Second, morphologically realistic multicompartment models are studied to investigate the passive properties of MN5. The passive electrical parameters fall in a range that is commonly observed in neurons, MN5 is spatially not compact, but for the single subtrees synaptic efficacy is location independent. Further, different subtrees are electrically independent from each other. Third, a continuum approach is used to formulate a new cable theoretic model to study the output in a dendritic cable with many subtrees, both analytically and computationally. The model is validated, by comparing it to a corresponding model with discrete branches. Further, the approach is demonstrated using MN5 and used to investigate spatially distributions of voltage gated ion channels.
This project explores the limits and legitimacy of neuroimaging as a means of understanding behavior and culpability in determining appropriate criminal sentencing. It highlights key philosophical issues surrounding the ability to use neuroimaging to support this process, and proposes a method of ensuring their proper use. By engaging case studies and a thought experiment, this project illustrates the circumstances in which neuroimaging may assist in identifying particular characteristics relevant for criminal sentencing.
I argue that it is not a question of whether or not neuroimaging itself holds validity in determining a criminals guilt or motives, but rather a proper application of the issue is to focus on the way in which information regarding these images is communicated from the `expert' scientists to the `non-expert' making decisions about the sentence that are most important. Those who are considering this information's relevance, a judge or jury, are typically not well versed in criminal neuroscience and interpreting the significance of different images. I advocate the way in which this information is communicated from the scientist-informer to the decision-maker parallels in importance to its actual meaning.
As a solution, I engage Roger Pielke's model of honest brokering as a solution to ensure the appropriate use of neuroimaging in determining criminal responsibility and sentencing. A thought experiment follows to highlight the limits of science, engage philosophical repercussions, and illustrate honest brokering as a means of resolution. To achieve this, a hypothetical dialogue reminiscent of Kenneth Schaffner's `tools for talking' with behavioral geneticists and courtroom professionals will exemplify these ideas.
Auditory hallucinations are a characteristic symptom of schizophrenia. Research has documented that the auditory cortex is metabolically activated when this process occurs, and that imbalances in the dopaminergic transmission in the striatum contribute to its physiopathology. Most animal models have focused the effort on pharmacological approaches like non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists to produce activation of the auditory cortex, or dopamine antagonists to alleviate it. I hypothesize that these perceptual phenomena can be explained by an imbalance activation of spiny projecting neurons in the striatal pathways, whereby supersensitive postsynaptic D2-like receptor, signaling in the posterior caudatoputamen generates activation of the auditory cortex. Therefore, I characterized the neuroanatomical component involved in the activation of the auditory cortex. I evaluated the participation of dopamine D2-like receptor using selective dopamine antagonist manipulations and identified the circuits related to the auditory cortex by retrograde trans-synaptic tracing using pseudorabies virus (PRV-152). My results show that dopamine infused in the posterior caudatoputamen dose dependently increases the transcription of the immediate early gene, zif268 in the auditory cortex, predominantly in layers III and IV, but also in cortical columns, suggesting enhanced functional auditory activity. This indicates the participation of the posterior striatum in the modulation of the secondary auditory cortex. I was able to demonstrate also that a coinfusion of a selective dopamine D2-like receptor antagonist, eticlopride and dopamine, attenuate the activation of the auditory cortex. Furthermore, using PRV-152 I delineate the distinctive circuit by axial mapping of the infected neurons. Thus, I found secondary projections from the posterior caudatoputamen that synapse in the thalamus before reaching the auditory cortex. These striatal projections correspond to the same brain region affected by dopamine during auditory cortical activation. My results further characterized a mechanism to generate intrinsic perception of sound that may be responsible for auditory hallucinations. I propose this paradigm may elucidate insight on the biological basis of psychotic behavior.