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- All Subjects: Neurosciences
- Creators: Greger, Bradley
Description
The brain is a fundamental target of the stress response that promotes adaptation and survival but the repeated activation of the stress response has the potential alter cognition, emotion, and motivation, key functions of the limbic system. Three structures of the limbic system in particular, the hippocampus, medial prefrontal cortex (mPFC), and amygdala, are of special interest due to documented structural changes and their implication in post-traumatic stress disorder (PTSD). One of many notable chronic stress-induced changes include dendritic arbor restructuring, which reflect plasticity patterns in parallel with the direction of alterations observed in functional imaging studies in PTSD patients. For instance, chronic stress produces dendritic retraction in the hippocampus and mPFC, but dendritic hypertrophy in the amygdala, consistent with functional imaging in patients with PTSD. Some have hypothesized that these limbic region's modifications contribute to one's susceptibility to develop PTSD following a traumatic event. Consequently, we used a familiar chronic stress procedure in a rat model to create a vulnerable brain that might develop traits consistent with PTSD when presented with a challenge. In adult male rats, chronic stress by wire mesh restraint (6h/d/21d) was followed by a variety of behavioral tasks including radial arm water maze (RAWM), fear conditioning and extinction, and fear memory reconsolidation to determine chronic stress effects on behaviors mediated by these limbic structures. In chapter 2, we corroborated past findings that chronic stress caused hippocampal CA3 dendritic retraction. Importantly, we present new findings that CA3 dendritic retraction corresponded with poor spatial memory in the RAWM and that these outcomes reversed after a recovery period. In chapter 3, we also showed that chronic stress impaired mPFC-mediated extinction memory, findings that others have reported. Using carefully assessed behavior, we present new findings that chronic stress impacted nonassociative fear by enhancing contextual fear during extinction that generalized to a new context. Moreover, the generalization behavior corresponded with enhanced functional activation in the hippocampus and amygdala during fear extinction memory retrieval. In chapter 5, we showed for the first time that chronic stress enhanced amygdala functional activation during fear memory retrieval, i.e., reactivation. Moreover, these enhanced fear memories were resistant to protein synthesis interference to disrupt a previously formed memory, called reconsolidation in a novel attempt to weaken chronic stress enhanced traumatic memory. Collectively, these studies demonstrated the plastic and dynamic effects of chronic stress on limbic neurocircuitry implicated in PTSD. We showed that chronic stress created a structural and functional imbalance across the hippocampus, mPFC, and amygdala, which lead to a PTSD-like phenotype with persistent and exaggerated fear following fear conditioning. These behavioral disruptions in conjunction with morphological and functional imaging data reflect a chronic stress-induced imbalance between hippocampal and mPFC regulation in favor of amygdala function overdrive, and supports a novel approach for traumatic memory processing in PTSD.
ContributorsHoffman, Ann (Author) / Conrad, Cheryl D. (Thesis advisor) / Olive, M. Foster (Committee member) / Hammer, Jr., Ronald P. (Committee member) / Sanabria, Federico (Committee member) / Arizona State University (Publisher)
Created2013
Description
Chronic restraint stress impairs hippocampal-mediated spatial learning and memory, which improves following a post-stress recovery period. Here, we investigated whether brain derived neurotrophic factor (BDNF), a protein important for hippocampal function, would alter the recovery from chronic stress-induced spatial memory deficits. Adult male Sprague-Dawley rats were infused into the hippocampus with adeno- associated viral vectors containing the coding sequence for short interfering (si)RNA directed against BDNF or a scrambled sequence (Scr), with both containing the coding information for green fluorescent protein to aid in anatomical localization. Rats were then chronically restrained (wire mesh, 6h/d/21d) and assessed for spatial learning and memory using a radial arm water maze (RAWM) either immediately after stressor cessation (Str-Imm) or following a 21-day post-stress recovery period (Str-Rec). All groups learned the RAWM task similarly, but differed on the memory retention trial. Rats in the Str-Imm group, regardless of viral vector contents, committed more errors in the spatial reference memory domain than did non-stressed controls. Importantly, the typical improvement in spatial memory following recovery from chronic stress was blocked with the siRNA against BDNF, as Str-Rec-siRNA performed worse on the RAWM compared to the non-stressed controls or Str-Rec-Scr. These effects were specific for the reference memory domain as repeated entry errors that reflect spatial working memory were unaffected by stress condition or viral vector contents. These results demonstrate that hippocampal BDNF is necessary for the recovery from stress-induced hippocampal dependent spatial memory deficits in the reference memory domain.
ContributorsOrtiz, J. Bryce (Author) / Conrad, Cheryl D. (Thesis advisor) / Olive, M. Foster (Committee member) / Taylor, Sara (Committee member) / Bimonte-Nelson, Heather A. (Committee member) / Arizona State University (Publisher)
Created2013
Description
Autism spectrum disorder (ASD) is a developmental neuropsychiatric condition with early childhood onset, thus most research has focused on characterizing brain function in young individuals. Little is understood about brain function differences in middle age and older adults with ASD, despite evidence of persistent and worsening cognitive symptoms. Functional Magnetic Resonance Imaging (MRI) in younger persons with ASD demonstrate that large-scale brain networks containing the prefrontal cortex are affected. A novel, threshold-selection-free graph theory metric is proposed as a more robust and sensitive method for tracking brain aging in ASD and is compared against five well-accepted graph theoretical analysis methods in older men with ASD and matched neurotypical (NT) participants. Participants were 27 men with ASD (52 +/- 8.4 years) and 21 NT men (49.7 +/- 6.5 years). Resting-state functional MRI (rs-fMRI) scans were collected for six minutes (repetition time=3s) with eyes closed. Data was preprocessed in SPM12, and Data Processing Assistant for Resting-State fMRI (DPARSF) was used to extract 116 regions-of-interest defined by the automated anatomical labeling (AAL) atlas. AAL regions were separated into six large-scale brain networks. This proposed metric is the slope of a monotonically decreasing convergence function (Integrated Persistent Feature, IPF; Slope of the IPF, SIP). Results were analyzed in SPSS using ANCOVA, with IQ as a covariate. A reduced SIP was in older men with ASD, compared to NT men, in the Default Mode Network [F(1,47)=6.48; p=0.02; 2=0.13] and Executive Network [F(1,47)=4.40; p=0.04; 2=0.09], a trend in the Fronto-Parietal Network [F(1,47)=3.36; p=0.07; 2=0.07]. There were no differences in the non-prefrontal networks (Sensory motor network, auditory network, and medial visual network). The only other graph theory metric to reach significance was network diameter in the Default Mode Network [F(1,47)=4.31; p=0.04; 2=0.09]; however, the effect size for the SIP was stronger. Modularity, Betti number, characteristic path length, and eigenvalue centrality were all non-significant. These results provide empirical evidence of decreased functional network integration in pre-frontal networks of older adults with ASD and propose a useful biomarker for tracking prognosis of aging adults with ASD to enable more informed treatment, support, and care methods for this growing population.
ContributorsCatchings, Michael Thomas (Author) / Braden, Brittany B (Thesis advisor) / Greger, Bradley (Thesis advisor) / Schaefer, Sydney (Committee member) / Arizona State University (Publisher)
Created2019
Description
Growing understanding of the neural code and how to speak it has allowed for notable advancements in neural prosthetics. With commercially-available implantable systems with bi- directional neural communication on the horizon, there is an increasing imperative to develop high resolution interfaces that can survive the environment and be well tolerated by the nervous system under chronic use. The sensory encoding aspect optimally interfaces at a scale sufficient to evoke perception but focal in nature to maximize resolution and evoke more complex and nuanced sensations. Microelectrode arrays can maintain high spatial density, operating on the scale of cortical columns, and can be either penetrating or non-penetrating. The non-penetrating subset sits on the tissue surface without puncturing the parenchyma and is known to engender minimal tissue response and less damage than the penetrating counterpart, improving long term viability in vivo. Provided non-penetrating microelectrodes can consistently evoke perception and maintain a localized region of activation, non-penetrating micro-electrodes may provide an ideal platform for a high performing neural prosthesis; this dissertation explores their functional capacity.
The scale at which non-penetrating electrode arrays can interface with cortex is evaluated in the context of extracting useful information. Articulate movements were decoded from surface microelectrode electrodes, and additional spatial analysis revealed unique signal content despite dense electrode spacing. With a basis for data extraction established, the focus shifts towards the information encoding half of neural interfaces. Finite element modeling was used to compare tissue recruitment under surface stimulation across electrode scales. Results indicated charge density-based metrics provide a reasonable approximation for current levels required to evoke a visual sensation and showed tissue recruitment increases exponentially with electrode diameter. Micro-scale electrodes (0.1 – 0.3 mm diameter) could sufficiently activate layers II/III in a model tuned to striate cortex while maintaining focal radii of activated tissue.
In vivo testing proceeded in a nonhuman primate model. Stimulation consistently evoked visual percepts at safe current thresholds. Tracking perception thresholds across one year reflected stable values within minimal fluctuation. Modulating waveform parameters was found useful in reducing charge requirements to evoke perception. Pulse frequency and phase asymmetry were each used to reduce thresholds, improve charge efficiency, lower charge per phase – charge density metrics associated with tissue damage. No impairments to photic perception were observed during the course of the study, suggesting limited tissue damage from array implantation or electrically induced neurotoxicity. The subject consistently identified stimulation on closely spaced electrodes (2 mm center-to-center) as separate percepts, indicating sub-visual degree discrete resolution may be feasible with this platform. Although continued testing is necessary, preliminary results supports epicortical microelectrode arrays as a stable platform for interfacing with neural tissue and a viable option for bi-directional BCI applications.
The scale at which non-penetrating electrode arrays can interface with cortex is evaluated in the context of extracting useful information. Articulate movements were decoded from surface microelectrode electrodes, and additional spatial analysis revealed unique signal content despite dense electrode spacing. With a basis for data extraction established, the focus shifts towards the information encoding half of neural interfaces. Finite element modeling was used to compare tissue recruitment under surface stimulation across electrode scales. Results indicated charge density-based metrics provide a reasonable approximation for current levels required to evoke a visual sensation and showed tissue recruitment increases exponentially with electrode diameter. Micro-scale electrodes (0.1 – 0.3 mm diameter) could sufficiently activate layers II/III in a model tuned to striate cortex while maintaining focal radii of activated tissue.
In vivo testing proceeded in a nonhuman primate model. Stimulation consistently evoked visual percepts at safe current thresholds. Tracking perception thresholds across one year reflected stable values within minimal fluctuation. Modulating waveform parameters was found useful in reducing charge requirements to evoke perception. Pulse frequency and phase asymmetry were each used to reduce thresholds, improve charge efficiency, lower charge per phase – charge density metrics associated with tissue damage. No impairments to photic perception were observed during the course of the study, suggesting limited tissue damage from array implantation or electrically induced neurotoxicity. The subject consistently identified stimulation on closely spaced electrodes (2 mm center-to-center) as separate percepts, indicating sub-visual degree discrete resolution may be feasible with this platform. Although continued testing is necessary, preliminary results supports epicortical microelectrode arrays as a stable platform for interfacing with neural tissue and a viable option for bi-directional BCI applications.
ContributorsOswalt, Denise (Author) / Greger, Bradley (Thesis advisor) / Buneo, Christopher (Committee member) / Helms-Tillery, Stephen (Committee member) / Mirzadeh, Zaman (Committee member) / Papandreou-Suppappola, Antonia (Committee member) / Arizona State University (Publisher)
Created2018
Description
Neural interfacing applications have advanced in complexity, with needs for increasingly high degrees of freedom in prosthetic device control, sharper discrimination in sensory percepts in bidirectional interfaces, and more precise localization of functional connectivity in the brain. As such, there is a growing need for reliable neurophysiological recordings at a fine spatial scale matching that of cortical columnar processing. Penetrating microelectrodes provide localization sufficient to isolate action potential (AP) waveforms, but often suffer from recorded signal deterioration linked to foreign body response. Micro-Electrocorticography (μECoG) surface electrodes elicit lower foreign body response and show greater chronic stability of recorded signals, though they typically lack the signal localization necessary to isolate individual APs. This dissertation validates the recording capacity of a novel, flexible, large area μECoG array with bilayer routing in a feline implant, and explores the ability of conventional μECoG arrays to detect features of neuronal activity in a very high frequency band associated with AP waveforms.
Recordings from both layers of the flexible μECoG array showed frequency features typical of cortical local field potentials (LFP) and were shown to be stable in amplitude over time. Recordings from both layers also showed consistent, frequency-dependent modulation after induction of general anesthesia, with large increases in beta and gamma band and decreases in theta band observed over three experiments. Recordings from conventional μECoG arrays over human cortex showed robust modulation in a high frequency (250-2000 Hz) band upon production of spoken words. Modulation in this band was used to predict spoken words with over 90% accuracy. Basal Ganglia neuronal AP firing was also shown to significantly correlate with various cortical μECoG recordings in this frequency band. Results indicate that μECoG surface electrodes may detect high frequency neuronal activity potentially associated with AP firing, a source of information previously unutilized by these devices.
Recordings from both layers of the flexible μECoG array showed frequency features typical of cortical local field potentials (LFP) and were shown to be stable in amplitude over time. Recordings from both layers also showed consistent, frequency-dependent modulation after induction of general anesthesia, with large increases in beta and gamma band and decreases in theta band observed over three experiments. Recordings from conventional μECoG arrays over human cortex showed robust modulation in a high frequency (250-2000 Hz) band upon production of spoken words. Modulation in this band was used to predict spoken words with over 90% accuracy. Basal Ganglia neuronal AP firing was also shown to significantly correlate with various cortical μECoG recordings in this frequency band. Results indicate that μECoG surface electrodes may detect high frequency neuronal activity potentially associated with AP firing, a source of information previously unutilized by these devices.
ContributorsBarton, Cody David (Author) / Greger, Bradley (Thesis advisor, Committee member) / Santello, Marco (Committee member) / Buneo, Christopher (Committee member) / Graudejus, Oliver (Committee member) / Artemiadis, Panagiotis (Committee member) / Arizona State University (Publisher)
Created2018
Description
The RAS/MAPK (RAS/Mitogen Activated Protein Kinase) pathway is a highly conserved, canonical signaling cascade that is highly involved in cellular growth and proliferation as well as cell migration. As such, it plays an important role in development, specifically in development of the nervous system. Activation of ERK is indispensable for the differentiation of Embryonic Stem Cells (ESC) into neuronal precursors (Li z et al, 2006). ERK signaling has also shown to mediate Schwann cell myelination of the peripheral nervous system (PNS) as well as oligodendrocyte proliferation (Newbern et al, 2011). The class of developmental disorders that result in the dysregulation of RAS signaling are known as RASopathies. The molecular and cell-specific consequences of these various pathway mutations remain to be elucidated. While there is evidence for altered DNA transcription in RASopathies, there is little work examining the effects of the RASopathy-linked mutations on protein translation and post-translational modifications in vivo. RASopathies have phenotypic and molecular similarities to other disorders such as Fragile X Syndrome (FXS) and Tuberous Sclerosis (TSC) that show evidence of aberrant protein synthesis and affect related pathways. There are also well-defined downstream RAS pathway elements involved in translation. Additionally, aberrant corticospinal axon outgrowth has been observed in disease models of RASopathies (Xing et al, 2016). For these reasons, this present study examines a subset of proteins involved in translation and translational regulation in the context of RASopathy disease states. Results indicate that in both of the tested RASopathy model systems, there is altered mTOR expression. Additionally the loss of function model showed a decrease in rps6 activation. This data supports a role for the selective dysregulation of translational control elements in RASopathy models. This data also indicates that the primary candidate mechanism for control of altered translation in these modes is through the altered expression of mTOR.
ContributorsHilbert, Alexander Robert (Author) / Newbern, Jason (Thesis director) / Olive, M. Foster (Committee member) / Bjorklund, Reed (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
Intracranial pressure is an important parameter to monitor, and elevated intracranial pressure can be life threatening. Elevated intracranial pressure is indicative of distress in the brain attributed by conditions such as aneurysm, traumatic brain injury, brain tumor, hydrocephalus, stroke, or meningitis.
Electrocorticography (ECoG) recordings are invaluable in understanding epilepsy and detecting seizure zones. However, ECoG electrodes cause a foreign body mass effect, swelling, and pneumocephaly, which results in elevation of intracranial pressure (ICP). Thus, the aim of this work is to design an intracranial pressure monitoring system that could augment ECoG electrodes.
A minimally invasive, low-cost epidural intracranial pressure monitoring system is developed for this purpose, using a commercial pressure transducer available for biomedical applications. The system is composed of a pressure transducer, sensing cup, electronics, and data acquisition system. The pressure transducer is a microelectromechanical system (MEMS)-based die that works on piezoresistive phenomenon with dielectric isolation for direct contact with fluids.
The developed system was bench tested and verified in an animal model to confirm the efficacy of the system for intracranial pressure monitoring. The system has a 0.1 mmHg accuracy and a 2% error for the 0-10 mmHg range, with resolution of 0.01 mmHg. This system serves as a minimally invasive (2 mm burr hole) epidural ICP monitor, which could augment existing ECoG electrode arrays, to simultaneously measure intracranial pressure along with the neural signals.
This device could also be employed with brain implants that causes elevation in ICP due to tissue - implant interaction often leading to edema. This research explores the concept and feasibility for integrating the sensing component directly on to the ECoG electrode arrays.
Electrocorticography (ECoG) recordings are invaluable in understanding epilepsy and detecting seizure zones. However, ECoG electrodes cause a foreign body mass effect, swelling, and pneumocephaly, which results in elevation of intracranial pressure (ICP). Thus, the aim of this work is to design an intracranial pressure monitoring system that could augment ECoG electrodes.
A minimally invasive, low-cost epidural intracranial pressure monitoring system is developed for this purpose, using a commercial pressure transducer available for biomedical applications. The system is composed of a pressure transducer, sensing cup, electronics, and data acquisition system. The pressure transducer is a microelectromechanical system (MEMS)-based die that works on piezoresistive phenomenon with dielectric isolation for direct contact with fluids.
The developed system was bench tested and verified in an animal model to confirm the efficacy of the system for intracranial pressure monitoring. The system has a 0.1 mmHg accuracy and a 2% error for the 0-10 mmHg range, with resolution of 0.01 mmHg. This system serves as a minimally invasive (2 mm burr hole) epidural ICP monitor, which could augment existing ECoG electrode arrays, to simultaneously measure intracranial pressure along with the neural signals.
This device could also be employed with brain implants that causes elevation in ICP due to tissue - implant interaction often leading to edema. This research explores the concept and feasibility for integrating the sensing component directly on to the ECoG electrode arrays.
ContributorsSampath Kumaran, Ranjani (Author) / Christen, Jennifer Blain (Thesis advisor) / Tillery, Stephen Helms (Committee member) / Greger, Bradley (Committee member) / Arizona State University (Publisher)
Created2015
Description
Evidence from the 20th century demonstrated that early life stress (ELS) produces long lasting neuroendocrine and behavioral effects related to an increased vulnerability towards psychiatric illnesses such as major depressive disorder, post-traumatic stress disorder, schizophrenia, and substance use disorder. Substance use disorders (SUDs) are complex neurological and behavioral psychiatric illnesses. The development, maintenance, and relapse of SUDs involve multiple brain systems and are affected by many variables, including socio-economic and genetic factors. Pre-clinical studies demonstrate that ELS affects many of the same systems, such as the reward circuitry and executive function involved with addiction-like behaviors. Previous research has focused on cocaine, ethanol, opiates, and amphetamine, while few studies have investigated ELS and methamphetamine (METH) vulnerability. METH is a highly addictive psychostimulant that when abused, has deleterious effects on the user and society. However, a critical unanswered question remains; how do early life experiences modulate both neural systems and behavior in adulthood? The emerging field of neuroepigenetics provides a potential answer to this question. Methyl CpG binding protein 2 (MeCP2), an epigenetic tag, has emerged as one possible mediator between initial drug use and the transition to addiction. Additionally, there are various neural systems that undergo long lasting epigenetics changes after ELS, such as the response of the hypothalamo-pituitary-adrenal (HPA) axis to stressors. Despite this, little attention has been given to the interactions between ELS, epigenetics, and addiction vulnerability. The studies described herein investigated the effects of ELS on METH self-administration (SA) in adult male rats. Next, we investigated the effects of ELS and METH SA on MeCP2 expression in the nucleus accumbens and dorsal striatum. Additionally, we investigated the effects of virally-mediated knockdown of MeCP2 expression in the nucleus accumbens core on METH SA, motivation to obtain METH under conditions of increasing behavioral demand, and reinstatement of METH-seeking in rats with and without a history of ELS. The results of these studies provide insights into potential epigenetic mechanisms by which ELS can produce an increased vulnerability to addiction in adulthood. Moreover, these studies shed light on possible novel molecular targets for treating addiction in individuals with a history of ELS.
ContributorsLewis, Candace (Author) / Olive, M. Foster (Thesis advisor) / Hammer, Ronald (Committee member) / Neisewander, Janet (Committee member) / Sanabria, Federico (Committee member) / Arizona State University (Publisher)
Created2015
Description
In the last 15 years, there has been a significant increase in the number of motor neural prostheses used for restoring limb function lost due to neurological disorders or accidents. The aim of this technology is to enable patients to control a motor prosthesis using their residual neural pathways (central or peripheral). Recent studies in non-human primates and humans have shown the possibility of controlling a prosthesis for accomplishing varied tasks such as self-feeding, typing, reaching, grasping, and performing fine dexterous movements. A neural decoding system comprises mainly of three components: (i) sensors to record neural signals, (ii) an algorithm to map neural recordings to upper limb kinematics and (iii) a prosthetic arm actuated by control signals generated by the algorithm. Machine learning algorithms that map input neural activity to the output kinematics (like finger trajectory) form the core of the neural decoding system. The choice of the algorithm is thus, mainly imposed by the neural signal of interest and the output parameter being decoded. The various parts of a neural decoding system are neural data, feature extraction, feature selection, and machine learning algorithm. There have been significant advances in the field of neural prosthetic applications. But there are challenges for translating a neural prosthesis from a laboratory setting to a clinical environment. To achieve a fully functional prosthetic device with maximum user compliance and acceptance, these factors need to be addressed and taken into consideration. Three challenges in developing robust neural decoding systems were addressed by exploring neural variability in the peripheral nervous system for dexterous finger movements, feature selection methods based on clinically relevant metrics and a novel method for decoding dexterous finger movements based on ensemble methods.
ContributorsPadmanaban, Subash (Author) / Greger, Bradley (Thesis advisor) / Santello, Marco (Committee member) / Helms Tillery, Stephen (Committee member) / Papandreou-Suppappola, Antonia (Committee member) / Crook, Sharon (Committee member) / Arizona State University (Publisher)
Created2017
Description
Prosthetic users abandon devices due to difficulties performing tasks without proper graded or interpretable feedback. The inability to adequately detect and correct error of the device leads to failure and frustration. In advanced prostheses, peripheral nerve stimulation can be used to deliver sensations, but standard schemes used in sensorized prosthetic systems induce percepts inconsistent with natural sensations, providing limited benefit. Recent uses of time varying stimulation strategies appear to produce more practical sensations, but without a clear path to pursue improvements. This dissertation examines the use of physiologically based stimulation strategies to elicit sensations that are more readily interpretable. A psychophysical experiment designed to investigate sensitivities to the discrimination of perturbation direction within precision grip suggests that perception is biomechanically referenced: increased sensitivities along the ulnar-radial axis align with potential anisotropic deformation of the finger pad, indicating somatosensation uses internal information rather than environmental. Contact-site and direction dependent deformation of the finger pad activates complimentary fast adapting and slow adapting mechanoreceptors, exhibiting parallel activity of the two associate temporal patterns: static and dynamic. The spectrum of temporal activity seen in somatosensory cortex can be explained by a combined representation of these distinct response dynamics, a phenomenon referred in this dissertation to “biphasic representation.” In a reach-to-precision-grasp task, neurons in somatosensory cortex were found to possess biphasic firing patterns in their responses to texture, orientation, and movement. Sensitivities seem to align with variable deformation and mechanoreceptor activity: movement and smooth texture responses align with potential fast adapting activation, non-movement and coarse texture responses align with potential increased slow adapting activation, and responses to orientation are conceptually consistent with coding of tangential load. Using evidence of biphasic representations’ association with perceptual priorities, gamma band phase locking is used to compare responses to peripheral nerve stimulation patterns and mechanical stimulation. Vibrotactile and punctate mechanical stimuli are used to represent the practical and impractical percepts commonly observed in peripheral nerve stimulation feedback. Standard patterns of constant parameters closely mimic impractical vibrotactile stimulation while biphasic patterns better mimic punctate stimulation and provide a platform to investigate intragrip dynamics representing contextual activation.
ContributorsTanner, Justin Cody (Author) / Helms Tillery, Stephen I (Thesis advisor) / Santos, Veronica J (Committee member) / Santello, Marco (Committee member) / Greger, Bradley (Committee member) / Buneo, Christopher A (Committee member) / Arizona State University (Publisher)
Created2017