Doctor of Philosophy, University of Akron, 2023, Biology

Vision is a crucial sense. Sight enables us to navigate and interact with our surroundings. Our environments contain an almost infinite variety of shapes, contours, and colors. Yet we only have a finite number of cells, and those cells consume a finite amount of energy. Vision enables us to effectively interact with these complex environments despite these limitations. In order for retinal development to be completed, light-evoked activity is required. Various synapses in the inner retina also must be established in order for these signals to propagate further. Only after these things occur can the visual system function at full capacity. Because of this much of the aims center around timing of electrophysiological activity in the retina. The first aim of this dissertation will be to establish a timeline for which photoreceptors (rods and cones), and bipolar cells are capable of generating and transmitting light evoked activity. Disruption of this light evoked activity can result in residual immature and can result in visual deficits. The second aim of this dissertation will be to analyze a model of X-linked retinoschisis at timepoints before eye-opening and determine how cells physiological output is reduced by this disease. The transition and increasing influence of GABA occurs around the same time we have determined bipolar cells become capable of light-evoked activity. The final aim of this dissertation is to describe a computational model of the generation and propagation of retinal waves from the SAC. Together each aim is directed at synaptogenesis at and around eye-opening. How does the presence of light evoked activity alter the physiological output of electrochemical signals at the first synapse and beyond, and how do these signals influence early synaptic refinement due to retinal waves?

PhD, University of Cincinnati, 2019, Arts and Sciences: Philosophy

Since Timothy van Gelder's 1995 paper “What Might Cognition be if not Computation?” there has been a growing distrust of representational accounts of cognition, most notably from proponents of relatively new programs like dynamical systems theory and ecological/embodied approaches to cognition. Some advocates of these programs have argued that the concept of “representation” is deeply flawed – does little explanatory work, prejudices what is researched and how results are interpreted, and loses sight of the complex interactions that hold between agents and their environments. In this dissertation, I will not try to challenge these claims. Instead, I will argue that responses from defenders of representational modeling often fail to adequately meet these challenges, underestimate their insights, and have a tendency to react by redefining “representation” in such a way that it loses its explanatory significance. Although I believe that the ultimate shape and utility of representational models of cognition will only be revealed in the course of doing science, I will advocate a new tack for defending representational modeling. I begin by acknowledging that representational terminology is indeed used inconsistently, and sometimes without warrant or explanatory power. Next, I examine cases from the cognitive neuroscience to try to show that we can distinguish between explanations whose representational features are closely tied to their explanatory ambitions and those that are not. I will argue that the representationalist should emphasize that information-processing solutions are contingent strategies available to organisms for producing adaptive behavior – as are varieties of synergistic agent-environmental coupling – and, therefore, there should be ways of marshaling evidence for or against the hypothesis that any particular cognitive/perceptual capacity is the result of a representational solution. She can then point out that explanatory representational models in neu (open full item for complete abstract)

MARCH, University of Cincinnati, 2016, Design, Architecture, Art and Planning: Architecture

Architects have long been uncertain about how the spaces and buildings they design affect the people who inhabit these environments on a neurological level. Regardless of this, mankind has long been the biological byproduct of our environmental context and the spaces we inhabit throughout our lives. Fred H. Gage, professor and Research Chair on Age-Related Neurodegenerative Diseases at the Laboratory of Genetics of the Salk Institute, wrote the following in a forward to John P. Eberhard's book Brain Landscape: The Coexistence of Neuroscience and Architecture: "I contend that architectural design can change our brains and behavior. The structures in the environment?the houses we live in, the areas we play in, the buildings we work in?affect our brains and our brains affect our behavior. By designing the structures we live in, architects are affecting our brains. The different spaces in which we live and work are changing our brain structures and our behaviors, and this has been going on for a long time." In an era rich with expansive knowledge into the inner working of our brains and how they continuously develop, the architects of today are challenged to venture deeper in their understanding of design impact on the mind and the resultant development of their fellow man. By harnessing the knowledge of how architecture influences neurons of the brain, future architects can employ a more sophisticated set of design tools to ensure that intended design outcomes result from their work.

PhD, University of Cincinnati, 2015, Arts and Sciences: Philosophy

Feminist philosophers of science identify sexist and androcentric science and develop alternate practices to address science's empirical limitations and its contributions to social oppression. However, some scholars have questioned the impact of feminist epistemology on scientific practice. In my dissertation, I advance the project of feminist philosophy of science by articulating a method to connect it to scientific practice. I develop a feminist philosophy of cognitive neuroscience using feminist standpoint empiricism that is informed by the specifics of practice. In chapter one, I establish the gap between feminist theory and feminist practice of science. I claim that feminist philosophy of science has the tools to effect change in scientific practice, but it must be articulated in a way that engages scientists. In order to make it relevant to scientists, feminist philosophy of science must be tailored to the specifics of a particular discipline of science. I defend feminist standpoint empiricism (Intemann 2010) for its potential to connect to scientific practice, and I identify the considerations for translating feminist standpoint empiricism to a specific science. In chapter two, I introduce the theory of sex/gender differences in the brain, the two neuroimaging case studies, and my critical approach: assessing the research on empirical grounds as well as through the feminist standpoint. The next two chapters are case studies on the neuroimaging of human sex or gender differences. Chapter three investigates structural differences in the corpus callosum, the white matter tract connecting the two hemispheres of the brain. The corpus callosum is thought to be larger and more bulbous in women. Chapter four investigates functional differences in a visuospatial task, mental rotation, a task in which men supposedly excel. Although many studies find sex or gender differences in the corpus callosum or in mental rotation activation, there are no consistent fin (open full item for complete abstract)

BA, Oberlin College, 2015, Mathematics

We study a family of discrete-time recurrent neural network models in which the synaptic connectivity changes slowly with respect to the neuronal dynamics. The fast (neuronal) dynamics of these models display a wealth of behaviors ranging from simple convergence and oscillation to chaos, and the addition of slow (synaptic) dynamics which mimic the biological mechanisms of learning and memory induces complex multiscale dynamics which render rigorous analysis quite difficult. Nevertheless, we prove a general result on the interplay of these two dynamical timescales, demarcating a regime of parameter space within which a gradual dampening of chaotic neuronal behavior is induced by a broad class of learning rules.

Doctor of Philosophy, The Ohio State University, 2011, Political Science

The problem of intentions is central to all major paradigms of international relations theory. Each paradigm has offered mechanisms by which intentions can be approximated, though not known. These mechanisms range from costly signaling in rationalism, iterative interaction in institutional liberalism, to reflected appraisals and identity in constructivism. Each of these perspectives involves agents observing the external behavior of actors and creating a theory about that behavior based on folk psychology reasoning. In this dissertation I present an alternate mechanism for understanding intentions that relies on simulating the intentions of others rather than theorizing about them. I argue that through face-to-face interaction actors are able to simulate the intentions of others, creating a one-to-one physical correspondence in the brain between individuals. This simulation allows actors to understand and replicate the intentions of others from an internal first-person perspective rather than an external third-person perspective. I investigate the implications of this finding for international relations theory, face-to-face diplomacy, and illustrate its effects empirically in diplomatic history.

Doctor of Philosophy, Case Western Reserve University, 2025, Biomedical Engineering

This dissertation focuses on non-perceptual effects of artificial sensation measured by effects in the motor system. Tactile feedback is used throughout the brain, from the “highest” cortical level to the “lower” spinal or brain stem level. Touch is first used before perception, or pre-perceptually, by the brain stem in simple, automatic modulation of the motor system. For example, carrying an object from place to place or even shifting it in one's hand involves many changing tactile signals. Even a single ridge of a fingertip supplies a unique signal for use in object manipulation. If one had to actively perceive and act upon all this information, merely picking up an object would become overwhelming. Fortunately, the lower levels of our brain automatically make minor adjustments to grip based on tactile information. What is not known is how relevant perceptual qualities are to these automatic corrections to grip. The cortex, not the brainstem, is the location of tactile perception, so it stands to reason that the brainstem does not require “natural” qualities of tactile feedback. Our lab has a group of participants with peripheral nerve cuff electrodes we can stimulation through. We tested how well artificial tactile feedback would integrate with the sensorimotor system in tasks of increasing complexity. We found that peripheral nerve stimulation is processed similarly to naturally generated touch with and without perception and may engage with the motor system as seen by the intent to modulate grip force.

Master of Science, The Ohio State University, 2008, Graduate School

Doctor of Philosophy, The Ohio State University, 2024, Neuroscience Graduate Studies Program

Background: Paternal deprivation is a significant early-life stressor with long-lasting effects on social behaviors and physiology. This series of studies investigates the extent to which paternal deprivation induces social impairments, alters corticosterone (CORT) reactivity, and affects central and peripheral immune responses in adult male and female offspring. We also examine the need for more research on the impact of paternal absence on offspring. Chapter 2 Hypothesis: Paternal deprivation induces social impairments, alterations in CORT reactivity, and changes in central immune response to acute stress in adult male and female offspring. Methods: We assessed the effects of paternal deprivation on social behaviors, CORT reactivity, and central immune response in adult California mice. Social behavior was evaluated using a novel same-sex and age-matched conspecific. CORT reactivity was measured following an acute physical stressor and central proinflammatory cytokine response was analyzed. Results: Paternal deprivation led to vigilant-avoidant social behavior in both male and female offspring, with social vigilance persisting in females but not in males. Paternally-deprived females exhibited reduced CORT reactivity, while males showed altered central proinflammatory cytokine response. Conclusion: These findings indicate that paternal deprivation induces more pronounced social impairments in female offspring, potentially mediated by sex-specific neurobiological mechanisms. Chapter 3. Hypothesis: Paternal deprivation results in sex-specific changes in social behaviors and basal neuroimmune function in adult offspring. Methods: A 30-minute social preference test was conducted to evaluate changes in social behaviors and social risk assessment strategies in paternally-deprived male and female California mice. Neuroinflammatory-related genes were assessed using NanoString nCounter technology to determine basal neuroimmune function. Results: Independent of rearing exper (open full item for complete abstract)

Doctor of Philosophy, The Ohio State University, 2024, Neuroscience Graduate Studies Program

Chronic stress is associated with the development of psychiatric disorders, including anxiety and post-traumatic stress disorder (PTSD). Inflammation is a key component of chronic stress and the development of psychiatric disorders. Repeated social defeat (RSD) is a rodent model of chronic stress that induces neuronal activation, microglial reactivity, and monocyte accumulation. RSD is associated with the development of anxiety-like behavior, social and cognitive deficits, and enhanced fear memory. RSD is clinically relevant as it shares key cellular and behavioral features with PTSD. Microglia play a key role in facilitating monocyte accumulation and anxiety-like behavior following RSD. Additionally, microglia have a primed profile 24d after the cessation of RSD, but how microglia mediate social and cognitive deficits or how microglia communicate with other cells after RSD is unknown. Therefore, single-cell(sc)RNAseq and single-nuclei(sn)RNAseq of the hippocampus was done 14h after RSD (Chapter 2). Here, novel stress-associated microglia were identified and uniquely characterized by cytokine/chemokine, EIF2, and phagocytotic signaling. Microglia depletion with PLX5622 (CSF1R inhibitor) prevented RSD-induced transcriptional changes to endothelia and astrocytes, but had limited, yet regionally specific effects on neurons. Furthermore, RSD-induced social withdrawal and cognitive impairment were microglia dependent. Collectively, these stress-associated microglia influenced transcriptional profiles in the hippocampus linked to social and cognitive deficits. RSD also induces stress-sensitization, where mice have amplified neuronal, immune, and behavioral responses to acute stress 24d later. The mechanisms underlying stress-sensitization are unclear. Thus, the next step of this study was to determine the influence of microglia and neuronal IL-1R1 (nIL-1R1) in stress-sensitization and fear memory after RSD (Chapter 3). Here, RSD enhanced fear memory acutely. Importantly, (open full item for complete abstract)

Master of Science (M.S.), University of Dayton, 2024, Biology

Intracellular Calcium (Ca2+) signaling plays a crucial role in a multitude of critical neuronal processes that range from cell development and long-term potentiation, to neurotransmission and programed cell death. One key regulator of intracellular Ca2+ handling is the Sarco/Endoplasmic Reticulum (ER) Ca2+ ATPase (SERCA) pump. SERCA is responsible for sequestering cytosolic Ca2+ into the ER, a major site for Ca2+ storage. Due to its importance in maintaining Ca2+ homeostasis, it comes as no surprise that dysfunction of SERCA has been shown to be involved in various neuropsychiatric diseases, such as Parkinson's Disease (PD), Alzheimer's Disease (AD), and Schizophrenia. Consequently, drugs that affect the function of SERCA are of high interest for future therapeutic treatments, but the role that SERCA plays in the brain and behavior is not well understood. In the context of the current thesis, we assessed the effects of chronic pharmacological SERCA activation using the drug CDN1163 on amino acidergic neurochemical responses and dendritic spine density in brain regions implicated in cognitive processes in mice of both sexes. Taken together, the findings of the current study provide initial insights into the role that SERCA activation may play the regulation of amino acidergic neurotransmission and synaptic plasticity, and provides the necessary premise needed to allow for more refined and targeted neurobiological assessments to understand the role of SERCA activation in the brain and behavior.

Doctor of Philosophy, Case Western Reserve University, 2024, EECS - Electrical Engineering

In this dissertation I present SNS-Toolbox, an open-source software package for the design and simulation of networks of biologically inspired neurons and synapses, also known as synthetic nervous systems (SNS). SNS-Toolbox allows SNS networks to be designed using a lightweight Python API, simulated in real-time on consumer computer hardware, and executed onboard physical robotic systems. I also present a companion package to SNS-Toolbox which allows simulation and training of large SNS networks using gradient backpropagation. This software is released under an open-source license with online documentation for ease of use, and has been disseminated to other researchers for their use. As a demonstration, I use SNS-Toolbox to implement a stereo visual motion detector, based on circuitry present within the \textit{Drosophila melanogaster} (fruit fly) optic lobe. This network analyzes local motion at each point within a visual field, and returns an estimate of global motion when subjected to grating stimuli. Finally I showcase the design of FlyWheel, a robotic benchmark for studying models of insect vision and applying SNS networks to physical hardware. This body of work marks the first tool which is capable of simulating SNS networks with hundreds to thousands of neurons and synaptic connections in real-time or faster, optimize networks with chemical reversal potentials using gradient backpropagation, and interface these networks for control of external systems.

Bachelor of Science (BS), Ohio University, 2024, Neuroscience

Duchene muscular dystrophy (DMD) is an X-Linked recessive genetic disorder which occurs in approximately 1/5000 XY births and is caused by a mutation in the human dystrophin gene. DMD causes many physiological defects and drastically shortens the lifespan of those afflicted by it. Gene replacement therapies are in clinical trials, but traditional therapies are still needed whilst those are developed. The C. elegans dys-1 gene is highly conserved compared to human dystrophin, and mutations in C. elegans dys-1 produces a clinically relevant phenotype. By use of the C. elegans DMD model, the pathology of DMD can easily be studied in a laboratory setting, allowing various potential traditional treatments to be tested for effectiveness. Zoledronic Acid (ZA) is approved by the U.S. Food and Drug Administration (FDA) to treat osteoporosis in patients with DMD, and preliminary data suggests that ZA could have positive effects for muscular health in DMD patients without osteoporosis. In the present work, it was found that the drug ZA is effective in improving DMD health in the C. elegans DMD model. Additionally, it was found that ZA improves DMD health through lowering the increased Ca2+ levels classically found in dys-1 mutants, which along with further experimentation informs a potential mechanistic pathway through which ZA acts. With this data, it is hoped that a clinical trial for repurposing ZA for use in for DMD patients is conducted in order to lessen the suffering caused by this disorder whilst gene therapeutics are developed.

Doctor of Philosophy, Case Western Reserve University, 2024, Genetics

Epilepsy is a neurological disorder characterized by repeated seizures. It affects 1% of the US population. Despite the recent progress in antiepileptic drug discovery and development, approximately 30% of the patients do not respond to current therapies. A major pitfall of the current antiepileptic drug discovery pipeline is current animal seizure models. The most widely used animal models are mechanically or chemically induced models, and they fail to recapitulate drug-resistant seizures, which are largely genetic epilepsies. Induced pluripotent stem cells (iPSCs) are promising alternative preclinical epilepsy models. iPSCs preserve the genetic information of epilepsy patients and can be an unlimited source of neuronal cell types of interest. Many studies have shown that iPSC disease models successfully reproduce epilepsy phenotypes. Herein, we successfully leveraged stem cell reprogramming technologies and CRISPR/Cas9 gene editing tools to generate iPSCs models of three drug-resistant epilepsies with monogenic cause: Early infantile epileptic encephalopathy, subtype 76 (EIEE-76), Microcephaly, Epilepsy, Diabetes Syndrome (MEDS), and GRIN2A-related epilepsy. Using these models, we uncovered pathophysiological mechanisms underlying the epilepsy phenotype of these rare genetic epilepsies that were previously unknown. We demonstrated EIEE-76 patient variant of ACTL6B dysregulates genes essential for neuronal development and that EIEE-76 patient-derived neurons demonstrated elevated electrophysiological activity than control, consistent with the patient phenotype. Also, we elucidated MEDS patient-derived neural progenitor cells (NPCs) have defects in secretory protein trafficking. Impaired protein trafficking during neurogenesis resulted in abnormal neuronal differentiation and electrophysiologically less active neuronal population. Next, we took a step further and developed a disease-relevant, high-throughput, phenotypic screen platform to identify potential an (open full item for complete abstract)

Doctor of Philosophy, The Ohio State University, 2023, Neuroscience Graduate Studies Program

Traumatic brain injury (TBI) is damage to the brain that is caused by an external force. As a leading cause of disabilities worldwide, TBIs can lead to long-term symptoms such as physical, cognitive, and psychological symptoms, including headaches, photosensitivity, seizures, attentional impairment, memory problems, impulsivity, increased anxiety, depression, and substance use disorders. Nearly 40% of TBI patients report two or more psychiatric symptoms after injury. Despite the high proportion of individuals that report psychiatric symptoms after TBI, there are no FDA-approved treatments for such impairments. Additionally, the mechanisms behind the development of psychiatric symptoms are poorly understood, but chronic neuroinflammation is believed to play an important role. Following injury, microglia propagate a chronic neuroinflammatory response that lasts years after the initial event and is linked to increases in psychiatric conditions. This work aimed to better understand the relationship between neuroinflammation and the development of psychiatric symptoms of lack of motivation, impulsivity, and inattention. First, it was examined if lipopolysaccharide (LPS) could model the chronic depressive-like symptoms (lack of motivation) of TBI to establish that long-term neuroinflammation leads to psychiatric symptoms. Motivation was measured with an operant task, the progressive ratio, which works by progressively increasing the effort required to earn a single reinforcer. A 14-day continuous LPS exposure (5 mg/kg/week) subcutaneously did not induce motivational deficits. LPS infused directly into the lateral ventricles (10.5 ug/kg/week) for 14 days caused a significant drop in motivation. However, this decrease in motivation did not mimic the effects of post-TBI depressive-like motivational impairments. Collectively demonstrating that chronic LPS cannot be used as a model for post-TBI depressive-like phenotypes. The next study focused on find (open full item for complete abstract)

Doctor of Philosophy, The Ohio State University, 2023, Psychology

This dissertation investigates the neural representation of complex social information by employing multivariate methods such as functional connectivity classification analyses and intersubject representational similarity analyses (IS-RSA). The present research examines the functional network associated with social interactions as well as the association between neural similarity and individual differences in emotional reactivity and empathy. Study 1 utilizes multivariate pattern analyses (MVPA) to classify different categories of social interactions based on connectivity patterns between brain regions involved in social perception. Study 2 uses IS-RSA to investigate how individual differences in emotional reactivity modulates the neural representation of different social interactions. Study 3 explores how idiosyncrasies in behavioral measures of empathy are associated with neural synchrony during the observation of naturalistic social scenes depicting specific characters and various types of interactions. Study 1 demonstrates that contextual categorical information about social interactions is better classified by a network of regions rather than within a single region of interest. Studies 2 and 3 suggest that idiosyncrasies in trait-like attributes such as empathy or emotional reactivity reflects differences in neural representation of complex social information. This research contributes to our understanding of how social information is processed in the brain and sheds light on the impact of individual differences on social perception.

PHD, Kent State University, 2023, College of Education, Health and Human Services / School of Health Sciences

Although speech recognition is often experienced as relatively effortless, there are a number of common challenges that can make speech perception more difficult and may greatly impact speech intelligibility (e.g., environmental noise). However, there is some indication that visual cues can be also used to improve speech recognition (Baratchu et al., 2008) — especially when the visual information is congruent with the speech signal (e.g., talking faces; Massaro, 2002). However, it is less clear how noisy visual environments may impact speech perception when the visual signal is not congruous with the speech signal. In fact, adding incongruous visual information will likely detract precious cognitive resources away from the auditory process, making speech perception in noise a more cognitively difficult task. Therefore, the purpose of this dissertation was to examine cognitive processing effort by measuring changes in pupillary response during the processing of speech in noise paired with incongruous visual noise. The primary hypothesis was that noisy visual information would negatively impact the processing of speech in noisy environments and that would result in a greater pupil diameter. To test this I used a common eye-tracking measure (i.e., pupillometry) to assess the cognitive processing effort needed to process speech in the presence of congruent and incongruous visual noise. The results indicated that visual noise recruits cognitive processing effort away from the auditory signal. Results also indicated that different combinations of auditory and visual noise have a significant impact on cognitive processing effort, which led to an increase in pupil dilation response during speech perception.

Doctor of Philosophy, The Ohio State University, 2023, Psychology

Why are some people successful at regulating their urges and cravings whereas others are more likely to give in to them? People use a variety of different self-regulation tools to achieve success. How these strategies change the way our brain processes information about food is not well understood. A goal of this research is to understand how different self-regulation strategies change the brain's response to food, which may help us understand why some people are good at controlling their eating behavior and others struggle with it. First, we generate a high quality image set suitable for use in a multivariate fMRI context (Chapter 2). Then, we investigate how shifting attention to different food attributes (Chapter 3) and how taking the perspective of a successful and unsuccessful self-regulator (Chapter 4) changes how the brain encodes important features of food like taste and health, and what areas support these changes. In addition to recording brain responses, we measure how often people make unhealthy or healthy food choices over the course of a week by texting them to complete short surveys on their smartphones. We find that changing one's attentional focus changes the dominant features that are represented in the brain's reward system. Further, we find that similarity towards a health-focused mindet predicts healthier food decisions in day-to-day-life. Mental simulation is found to change the way food information is organized, both cognitively and neurally. Additionally, we find that regions related to social congntion support these differences in representation. In so doing, this work provides some evidence of how the brain encodes the tastiness and healthiness of foods, and the regions supporting this representation, to help clarify good strategies for dietary self-control and ultimately to help populations that struggle with in this domain.

Doctor of Philosophy, Miami University, 2023, Psychology

Opioid Use Disorder (OUD) is a chronic relapsing brain disorder characterized by a variety of symptoms, including withdrawal. Withdrawal is a crucial point in the addiction cycle and is heavily involved in the susceptibility to relapse due to the strong negative affect, or aversion, that it brings about. However, both our understanding of the neurobiology of withdrawal-induced aversion as well as current treatment options are lacking. Most of our understanding of the neurobiology of withdrawal-induced aversion involves mesolimbic dopamine (DA) neurons and the regions that project to them. Because of their profound impact on DA release and expression of the mu opioid receptor (MOR), the cholinergic interneurons (CINs) of the striatum are one such population that has gained recent interest. In this dissertation, the activity of CINs was manipulated through both a transgenic and chemogenetic approach in mice, which revealed a crucial role CINs play in the expression of opioid withdrawal and self-administration, with some surprising sex differences. These studies provided novel information for the field, as no previous study had investigated the role of CINs in opioid withdrawal behaviors. Continuing this work is vital in our development of new therapeutic strategies for humans living with OUD.

BS, Kent State University, 2023, College of Arts and Sciences / Department of Anthropology

The endocannabinoid system plays an important role in social behaviors across a variety of species. Recently, the distribution of cannabinoid receptor 1 (CB1) was linked to the mating patterns of voles (i.e., monogamy versus non-monogamy) (Simmons et al., 2021). This raises the question of whether a similar mechanism exists in primates. The goal of the present study was to address that question by examining the relationship between CB1 density and mating patterns in monogamous (owl monkey, marmoset) and non-monogamous (capuchin) New World monkeys. Our study found that CB1 axon length density was higher in the monogamous species than the promiscuous in layer III of the anterior cingulate cortex. Our study suggests a potential correlation between monogamy and CB1 in New World monkeys. More research is needed to determine the extent of this trend in other primate species.