Matching Items (51)
Description

In the face of widespread pollinator decline, research has increasingly focused on ways that pesticides could be harming bees. Fungicides are pesticides that are used in greater volumes than insecticides, yet significantly fewer studies have investigated the effects of these agrochemicals. The fungicide Pristine® is commonly used on bee-pollinated crops

In the face of widespread pollinator decline, research has increasingly focused on ways that pesticides could be harming bees. Fungicides are pesticides that are used in greater volumes than insecticides, yet significantly fewer studies have investigated the effects of these agrochemicals. The fungicide Pristine® is commonly used on bee-pollinated crops and has been shown to be detrimental to physiological processes that are key to honey bee foraging, such as digestion and learning. This study seeks to investigate how Pristine® exposure affects the amount of water, nectar, and pollen that honey bees collect. Colonies were fed either plain pollen patties or pollen patties containing 23 ppm Pristine®. Exposure to fungicide had no significant effect on corbicular pollen mass, the crop volumes of nectar or water foragers, or the proportions of foragers collecting different substances. There was a significantly higher sugar concentration in the crop of Pristine®-exposed nectar foragers (43.6%, 95% CI [38.8, 48.4]) compared to control nectar foragers (36.3%, 95% CI [31.9, 40.6]). The higher sugar concentration in the nectar of Pristine®-treated bees could indicate that the agrochemical decreases sucrose responsiveness or nutritional status in bees. Alternatively, fungicide exposure may increase the amount of sugar that bees need to make it back to the hive. Based on these results, it would appear that fungicides like Pristine® do not strongly affect the amounts of substances that honey bees collect, but it is still highly plausible that treated bees forage more slowly or with lower return rates.

ContributorsChester, Elise (Author) / Harrison, Jon (Thesis director) / DesJardins, Nicole (Committee member) / Smith, Brian (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2023-05
Description
Active sensing is a sensory phenomenon in which organisms use self-generated energy to examine their surroundings. This experiment strives to better understand active sensing in honeybees, predicting that active sensing may display itself primarily through antennae movement and that preventing antennae movement may result in differences in electroantennogram dose-response curves

Active sensing is a sensory phenomenon in which organisms use self-generated energy to examine their surroundings. This experiment strives to better understand active sensing in honeybees, predicting that active sensing may display itself primarily through antennae movement and that preventing antennae movement may result in differences in electroantennogram dose-response curves and associative learning plasticity. This will be done by examining changes in amplitude in electroantennogram response in both fixed-antenna and free-antenna bees over the course of a differential training protocol that establishes learned behavior discrimination.
ContributorsLei, Harry (Author) / Smith, Brian (Thesis director) / Albin-Brooks, Christopher (Committee member) / Barrett, The Honors College (Contributor)
Created2023-05
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Description
By increasing the mean and variance of environmental temperatures, climate change has caused local extinctions and range shifts of numerous species. However, biologists disagree on which populations and species are most vulnerable to future warming. This debate arises because biologists do not know which physiological processes are most vulnerable to

By increasing the mean and variance of environmental temperatures, climate change has caused local extinctions and range shifts of numerous species. However, biologists disagree on which populations and species are most vulnerable to future warming. This debate arises because biologists do not know which physiological processes are most vulnerable to temperature or how to model these processes in complex environments. Using the South American locust (Schistocerca cancellata) as a model system, my dissertation addressed this debate and explained how climate limits the persistence of locust populations. Locusts of S. cancellata are serious agricultural pests with occasional outbreaks covering up to 4 million km2 over six countries. Because outbreaks are largely driven by climate, understanding how climate limits the persistence of locusts may help predict crop losses in future climates. To achieve this aim, I integrated observational, experimental, and computational approaches. First, I tested a physiological model of heat stress. By measuring the heat tolerance of locusts under different oxygen concentrations, I demonstrated that heat tolerance depends on oxygen supply during the hatchling stage only. Second, I modeled the geographic distribution of locusts using physiological traits. I started by measuring thermal effects on consumption and defecation of field-captured locusts, and I then used these data to model energy gain in current and future climates. My results indicated that incorporating physiological mechanisms can improve the accuracy of models and alter predicted impacts of climate change. Finally, I explored the causes and consequences of intraspecific variation in heat tolerance. After measuring heat tolerance of locusts in different hydration states and developmental stages, I modeled survival in historical microclimates. My models indicated that recent climate change has amplified the risk of overheating for locusts, and this risk depended strongly on shade availability, hydration state, and developmental stage. Therefore, the survival of locusts in future climates will likely depend on their access to shade and water. Overall, my dissertation argues that modeling physiological mechanisms can improve the ability of biologists to predict the impacts of climate change.
ContributorsYoungblood, Jacob (Author) / Angilletta, Michael (Thesis advisor) / Buckley, Lauren (Committee member) / Cease, Arianne (Committee member) / Smith, Brian (Committee member) / Vanden Brooks, John (Committee member) / Arizona State University (Publisher)
Created2022
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Description
Transorbital surgery has gained recent notoriety due to its incorporation into endoscopic skull base surgery. The body of published literature on the field is cadaveric and observation. The pre-clinical studies are focused on the use of the endoscope only. Furthermore the methodology utilised in the published literature is inconsistent and

Transorbital surgery has gained recent notoriety due to its incorporation into endoscopic skull base surgery. The body of published literature on the field is cadaveric and observation. The pre-clinical studies are focused on the use of the endoscope only. Furthermore the methodology utilised in the published literature is inconsistent and does not embody the optimal principles of scientific experimentation. This body of work evaluates a minimally invasive novel surgical corridor - the transorbital approach - its validity in neurosurgical practice, as well as both qualitatively and quantitatively assessing available technological advances in a robust experimental fashion. While the endoscope is an established means of visualisation used in clinical transorbital surgery, the microscope has never been assessed with respect to the transorbital approach. This question is investigated here and the anatomical and surgical benefits and limitations of microscopic visualisation demonstrated. The comparative studies provide increased knowledge on specifics pertinent to neurosurgeons and other skull base specialists when planning pre-operatively, such as pathology location, involved anatomical structures, instrument maneuvrability and the advantages and disadvantages of the distinct visualisation technologies. This is all with the intention of selecting the most suitable surgical approach and technology, specific to the patient, pathology and anatomy, so as to perform the best surgical procedure. The research findings illustrated in this body of work are diverse, reproducible and applicable. The transorbital surgical corridor has substantive potential for access to the anterior cranial fossa and specific surgical target structures. The neuroquantitative metrics investigated confirm the utility and benefits specific to the respective visualisation technologies i.e. the endoscope and microscope. The most appropriate setting wherein the approach should be used is also discussed. The transorbital corridor has impressive potential, can utilise all available technological advances, promotes multi-disciplinary co-operation and learning amongst clinicians and ultimately, is a means of improving operative patient care.
ContributorsHoulihan, Lena Mary (Author) / Preul, Mark C. (Thesis advisor) / Vernon, Brent (Thesis advisor) / O' Sullivan, Michael G.J. (Committee member) / Lawton, Michael T. (Committee member) / Santarelli, Griffin (Committee member) / Smith, Brian (Committee member) / Arizona State University (Publisher)
Created2021
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Description
Olfactory perception is a complex and multifaceted process that involves the detection of volatile organic compounds by olfactory receptor neurons in the nasal neuroepithelium. Different odorants can elicit different perceived intensities at the same concentration, while direct intensity ratings are vulnerable to framing effects and inconsistent scale usage. Odor perception

Olfactory perception is a complex and multifaceted process that involves the detection of volatile organic compounds by olfactory receptor neurons in the nasal neuroepithelium. Different odorants can elicit different perceived intensities at the same concentration, while direct intensity ratings are vulnerable to framing effects and inconsistent scale usage. Odor perception is genetically determined, with each individual having a unique olfaction "footprint" and sensitivity levels. Genetic factors, age, gender, race, and environmental factors influence olfactory acuity. The olfactory system's complexity makes it challenging to create a standardized comparison system for olfactory perception tests. The COVID-19 pandemic has underscored the importance of olfactory dysfunction, particularly the loss of smell and taste as common symptoms. Research has demonstrated the widespread occurrence of olfactory impairment in various populations, often stemming from post-viral origins, which is the leading cause of permanent smell loss. Utilizing quantitative ranking on a qualitative scale enhances the precision and accuracy when evaluating and drawing conclusions about odor perception and how to mitigate problems caused by external factors. Pairwise comparisons enhance the accuracy and consistency of results and provide a more intuitive way of comparing items. Such ranking techniques can lead to early detection of olfactory disorders and improved diagnostic tools. The COVID-19 pandemic has shed light on the significance of olfactory dysfunction, emphasizing the need for further research and standardized testing methods in olfactory perception.
ContributorsDarden, Jaelyn (Author) / Smith, Brian (Thesis advisor) / Gerkin, Richard (Thesis advisor) / Spackman, Christy (Committee member) / Arizona State University (Publisher)
Created2023
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Description
Development of the central nervous system is an incredible process that relies on multiple extracellular signaling cues and complex intracellular interactions. Approximately 1500 genes are associated with neurodevelopmental disorders, many of which are linked to a specific biochemical signaling cascade known as Extracellular-Signal Regulated Kinase (ERK1/2). Clearly defined mutations in

Development of the central nervous system is an incredible process that relies on multiple extracellular signaling cues and complex intracellular interactions. Approximately 1500 genes are associated with neurodevelopmental disorders, many of which are linked to a specific biochemical signaling cascade known as Extracellular-Signal Regulated Kinase (ERK1/2). Clearly defined mutations in regulators of the ERK1/2 pathway cause syndromes known as the RASopathies. Symptoms include intellectual disability, developmental delay, cranio-facial and cardiac deficits. Treatments for RASopathies are limited due to an in complete understanding of ERK1/2’s role in brain development. Individuals with Neurofibromatosis Type and Noonan Syndrome, the two most common RASopathies, exhibit aberrant functional and white matter organization in non-invasive imaging studies, however, the contributions of neuronal versus oligodendrocyte deficits to this phenotype are not fully understood. To define the cellular functions of ERK1/2 in motor circuit formation, this body of work focuses on two long-range projection neuron subtypes defined by their neurotransmitter. With genetic mouse models, pathological ERK1/2 in glutamatergic neurons reduces axonal outgrowth, resulting in deficits in activity dependent gene expression and the ability to learn a motor skill task. Restricting pathological ERK1/2 within cortical layer V recapitulates these wiring deficits but not the behavioral learning phenotype. Moreover, it is uncovered that pathological ERK1/2 results in compartmentalized expression pattern of phosphorylated ERK1/2. It is not clear whether ERK1/2 functions are similar in cholinergic neuron populations that mediate attention, memory, and motor control. Basal forebrain cholinergic neuron development relies heavily on NGF-TrKA neurotrophic signaling known to activate ERK1/2. Yet the function of ERK1/2 during cholinergic neuronal specification and differentiation is poorly understood. By selectively deleting ERK1/2 in cholinergic neurons, ERK1/2 is required for activity-dependent maturation of neuromuscular junctions in juvenile mice, but not the establishment of lower motor neuron number. Moreover, ERK1/2 is not required for specification of choline acetyltransferase expressing basal forebrain cholinergic neurons by 14 days of age. However, ERK1/2 may be necessary for BFCN maturation by adulthood. Collectively, these data indicate that glutamatergic neuron-autonomous decreases in long-range axonal outgrowth and modest effects on later stages of cholinergic neuron maintenance may be important aspects of neuropathogenesis in RASopathies.
ContributorsRees, Katherina Pavy (Author) / Newbern, Jason (Thesis advisor) / Olive, Foster (Committee member) / Qiu, Shenfeng (Committee member) / Sattler, Rita (Committee member) / Smith, Brian (Committee member) / Arizona State University (Publisher)
Created2024
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Description
The RASopathies are a collection of developmental diseases caused by germline mutations in components of the RAS/MAPK signaling pathway and is one of the world’s most common set of genetic diseases. A majority of these mutations result in an upregulation of RAS/MAPK signaling and cause a variety of both physical

The RASopathies are a collection of developmental diseases caused by germline mutations in components of the RAS/MAPK signaling pathway and is one of the world’s most common set of genetic diseases. A majority of these mutations result in an upregulation of RAS/MAPK signaling and cause a variety of both physical and neurological symptoms. Neurodevelopmental symptoms of the RASopathies include cognitive and motor delays, learning and intellectual disabilities, and various behavioral problems. Recent noninvasive imaging studies have detected widespread abnormalities within white matter tracts in the brains of RASopathy patients. These abnormalities are believed to be indicative of underlying connectivity deficits and a possible source of the behavioral and cognitive deficits. To evaluate these long-range connectivity and behavioral issues in a cell-autonomous manner, MEK1 loss- and gain-of-function (LoF and GoF) mutations were induced solely in the cortical glutamatergic neurons using a Nex:Cre mouse model. Layer autonomous effects of the cortex were also tested in the GoF mouse using a layer 5 specific Rbp4:Cre mouse. Immunohistochemical analysis showed that activated ERK1/2 (P-ERK1/2) was expressed in high levels in the axonal compartments and reduced levels in the soma when compared to control mice. Axonal tract tracing using a lipophilic dye and an adeno-associated viral (AAV) tract tracing vector, identified significant corticospinal tract (CST) elongation deficits in the LoF and GoF Nex:Cre mouse and in the GoF Rbp4:Cre mouse. AAV tract tracing was further used to identify significant deficits in axonal innervation of the contralateral cortex, the dorsal striatum, and the hind brain of the Nex:Cre GoF mouse and the contralateral cortex and dorsal striatum of the Rbp4:Cre mouse. Behavioral testing of the Nex:Cre GoF mouse indicated deficits in motor learning acquisition while the Rbp4:Cre GoF mouse showed no failure to acquire motor skills as tested. Analysis of the expression levels of the immediate early gene ARC in Nex:Cre and Rbp4:Cre mice showed a specific reduction in a cell- and layer-autonomous manner. These findings suggest that hyperactivation of the RAS/MAPK pathway in cortical glutamatergic neurons, induces changes to the expression patterns of P-ERK1/2, disrupts axonal elongation and innervation patterns, and disrupts motor learning abilities.
ContributorsBjorklund, George Reed (Author) / Newbern, Jason M (Thesis advisor) / Neisewander, Janet (Committee member) / Smith, Brian (Committee member) / Orchinik, Miles (Committee member) / Mangone, Marco (Committee member) / Arizona State University (Publisher)
Created2018
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Description
Cell morphology and the distribution of voltage gated ion channels play a major role in determining a neuron's firing behavior, resulting in the specific processing of spatiotemporal synaptic input patterns. Although many studies have provided insight into the computational properties arising from neuronal structure as well as from channel kinetics,

Cell morphology and the distribution of voltage gated ion channels play a major role in determining a neuron's firing behavior, resulting in the specific processing of spatiotemporal synaptic input patterns. Although many studies have provided insight into the computational properties arising from neuronal structure as well as from channel kinetics, no comprehensive theory exists which explains how the interaction of these features shapes neuronal excitability. In this study computational models based on the identified Drosophila motoneuron (MN) 5 are developed to investigate the role of voltage gated ion channels, the impact of their densities and the effects of structural features.

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.
ContributorsBerger, Sandra (Author) / Crook, Sharon (Thesis advisor) / Baer, Steven (Committee member) / Hamm, Thomas (Committee member) / Smith, Brian (Committee member) / Arizona State University (Publisher)
Created2014
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Description
Traumatic brain injury (TBI) most frequently occurs in pediatric patients and remains a leading cause of childhood death and disability. Mild TBI (mTBI) accounts for 70-90% of all TBI cases, yet its neuropathophysiology is still poorly understood. While a single mTBI injury can lead to persistent deficits, repeat injuries

Traumatic brain injury (TBI) most frequently occurs in pediatric patients and remains a leading cause of childhood death and disability. Mild TBI (mTBI) accounts for 70-90% of all TBI cases, yet its neuropathophysiology is still poorly understood. While a single mTBI injury can lead to persistent deficits, repeat injuries increase the severity and duration of both acute symptoms and long term deficits. In this study, to model pediatric repetitive mTBI (rmTBI) we subjected unrestrained juvenile animals (post-natal day 20) to repeat weight drop impact. Animals were anesthetized and subjected to sham or rmTBI once per day for 5 days. At 14 days post injury (PID), magnetic resonance imaging (MRI) revealed that rmTBI animals displayed marked cortical atrophy and ventriculomegaly. Specifically, the thickness of the cortex was reduced up to 46% beneath and the ventricles increased up to 970% beneath the impact zone. Immunostaining with the neuron specific marker NeuN revealed an overall loss of neurons within the motor cortex but no change in neuronal density. Examination of intrinsic and synaptic properties of layer II/III pyramidal neurons revealed no significant difference between sham and rmTBI animals at rest or under convulsant challenge with the potassium channel blocker, 4-Aminophyridine. Overall, our findings indicate that the neuropathological changes reported after pediatric rmTBI can be effectively modeled by repeat weight drop in juvenile animals. Developing a better understanding of how rmTBI alters the pediatric brain may help improve patient care and direct "return to game" decision making in adolescents.
ContributorsGoddeyne, Corey (Author) / Anderson, Trent (Thesis advisor) / Smith, Brian (Committee member) / Kleim, Jeffrey (Committee member) / Arizona State University (Publisher)
Created2014
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Description
Food is an essential driver of animal behavior. For social organisms, the acquisition of food guides interactions with the environment and with group-mates. Studies have focused on how social individuals find and choose food sources, and share both food and information with group-mates. However, it is often not clear how

Food is an essential driver of animal behavior. For social organisms, the acquisition of food guides interactions with the environment and with group-mates. Studies have focused on how social individuals find and choose food sources, and share both food and information with group-mates. However, it is often not clear how experiences throughout an individual's life influence such interactions. The core question of this thesis is how individuals’ experience contributes to within-caste behavioral variation in a social group. I investigate the effects of individual history, including physical injury and food-related experience, on individuals' social food sharing behavior, responses to food-related stimuli, and the associated neural biogenic amine signaling pathways. I use the eusocial honey bee (Apis mellifera) system, one in which individuals exhibit a high degree of plasticity in responses to environmental stimuli and there is a richness of communicatory pathways for food-related information. Foraging exposes honey bees to aversive experiences such as predation, con-specific competition, and environmental toxins. I show that foraging experience changes individuals' response thresholds to sucrose, a main component of adults’ diets, depending on whether foraging conditions are benign or aversive. Bodily injury is demonstrated to reduce individuals' appetitive responses to new, potentially food-predictive odors. Aversive conditions also impact an individual's social food sharing behavior; mouth-to-mouse trophallaxis with particular groupmates is modulated by aversive foraging conditions both for foragers who directly experienced these conditions and non-foragers who were influenced via social contact with foragers. Although the mechanisms underlying these behavioral changes have yet to be resolved, my results implicate biogenic amine signaling pathways as a potential component. Serotonin and octopamine concentrations are shown to undergo long-term change due to distinct foraging experiences. My work serves to highlight the malleability of a social individual's food-related behavior, suggesting that environmental conditions shape how individuals respond to food and share information with group-mates. This thesis contributes to a deeper understanding of inter-individual variation in animal behavior.
ContributorsFinkelstein, Abigail (Author) / Amdam, Gro V (Thesis advisor) / Conrad, Cheryl (Committee member) / Smith, Brian (Committee member) / Neisewander, Janet (Committee member) / Bimonte-Nelson, Heather A. (Committee member) / Arizona State University (Publisher)
Created2017