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Title: The application of opsins to control mitochondrial metabolism: Stage 1 – testing for the presence of opsins in the inner mitochondrial membranes of transgenic fruit flies.
Creator: Fontinelle, Gabriella, Macleod, Gregory, Harriet L. Wilkes Honors College
Abstract/Description: Mitochondrial dysfunction has been associated with the pathology of most neurodegenerative diseases. An essential element of mitochondrial function is a robust proton motive force (PMF) across the inner mitochondria membrane (IMM).
Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00003673
Format: Document (PDF)

Title: Nf1 Mutations Impair Memory-Related Plasticity in the Drosophila melanogaster Mushroom Body.
Creator: Gilliland, Brandon, Tomchik, Seth, Macleod, Gregory, Harriet L. Wilkes Honors College
Abstract/Description: The purpose of this project was to understand the effects of therapeutic antidepressants with respect to circadian rhythm in Drosophila melanogaster. Antidepressants are known to have a role in dopamine and serotonin signaling pathways. These pathways have been observed to have a role in circadian rhythm, the biological process involving sleep patterns. In the experiments completed thus far, it has been observed that the flies administered antidepressants have more fractioned sleep than the...
Show moreThe purpose of this project was to understand the effects of therapeutic antidepressants with respect to circadian rhythm in Drosophila melanogaster. Antidepressants are known to have a role in dopamine and serotonin signaling pathways. These pathways have been observed to have a role in circadian rhythm, the biological process involving sleep patterns. In the experiments completed thus far, it has been observed that the flies administered antidepressants have more fractioned sleep than the control group flies. It has also been noted that normal light to dark sleep cycles are altered significantly in the flies given antidepressants. It is important to research and to understand the effects of antidepressants in Drosophila melanogaster because it could lead to a more effective way to administer antidepressants to humans without harmful side effects.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00005191
Subject Headings: College students --Research --United States.
Format: Document (PDF)

Title: Apparatus for visual place learning through aversive conditioning in Drosophila melanogaster.
Creator: Alvarado, Christian, Macleod, Gregory, Florida Atlantic University, Harriet L. Wilkes Honors College
Abstract/Description: Learning and memory studies in Drosophila melanogaster have led to advances in understanding fly and mammalian genetics and neurophysiology. Despite extensive studies, there remain gaps in the scientific literature concerning genes and neural pathways involved in learning and memory. There are differences in the memory traces between olfactory and visual memory, yet visual learning has not been studied to the same extent as olfactory learning. Visual place learning has only recently been...
Show moreLearning and memory studies in Drosophila melanogaster have led to advances in understanding fly and mammalian genetics and neurophysiology. Despite extensive studies, there remain gaps in the scientific literature concerning genes and neural pathways involved in learning and memory. There are differences in the memory traces between olfactory and visual memory, yet visual learning has not been studied to the same extent as olfactory learning. Visual place learning has only recently been addressed. We offer a new apparatus for studying visual place learning in D. melanogaster. The new apparatus offers a compelling and cost-effective approach to investigating visual place learning. The most notable difference between the new apparatus and others designed for visual place learning is the use of Peltier units in conjunction with a hydraulic system to supply heat used as a negative stimulus, with the advantages of even heat distribution, ease of construction, and ease of operation.
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Date Issued: 2019
PURL: http://purl.flvc.org/fau/fd/FAUHT00067
Format: Document (PDF)

Title: MAPPING MITOCHONDRIAL NUMBER AND MORPHOLOGY IN THE BRAINS OF DROSOPHILA MELANOGASTER MODELS OF PARKINSON’S DISEASE.
Creator: Murphy, Regina, Macleod, Gregory, Florida Atlantic University, Harriet L. Wilkes Honors College
Abstract/Description: Parkinson’s Disease (PD) is a neurodegenerative disorder that affects millions of people around the world, although it is more common in individuals aged 60 years or older. PD is associated with the degeneration of dopamine neurons in the substantia nigra. While the underlying cause of neuronal degeneration is poorly understood, mitochondrial dysfunction is a common feature of the cell pathology. Geneticallyencoded fluorescent probes were used to label the mitochondria in wildtype Drosophila...
Show moreParkinson’s Disease (PD) is a neurodegenerative disorder that affects millions of people around the world, although it is more common in individuals aged 60 years or older. PD is associated with the degeneration of dopamine neurons in the substantia nigra. While the underlying cause of neuronal degeneration is poorly understood, mitochondrial dysfunction is a common feature of the cell pathology. Geneticallyencoded fluorescent probes were used to label the mitochondria in wildtype Drosophila melanogaster and those genetically manipulated to model PD. Brains were dissected, immunolabeled, and their mitochondria were imaged using structured illumination microscopy (SIM). Mitochondrial number was determined, as well as the sphericity and surface area quantified. This characterization of mitochondrial number and morphology in wildtype Drosophila created a baseline for comparison to Drosophila that over-express the wildtype human α-synuclein protein which is associated with PD.
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Date Issued: 2018
PURL: http://purl.flvc.org/fau/fd/FAUHT00032
Format: Document (PDF)

Title: ENVIRONMENTAL ENRICHMENT AND SOCIAL RECOGNITION IN PTEN+/- MICE.
Creator: Tygar, Farrah, Macleod, Gregory, Florida Atlantic University, Harriet L. Wilkes Honors College
Abstract/Description: Autism Spectrum Disorder (ASD) can be can be caused by numerous different genetic abnormalities, one of which is Pten haploinsufficiency. There is some evidence to suggest that environmental enrichment can decrease the symptoms of ASD and Pten mutant mice have been shown to have altered social behaviors. Therefore, Pten and WT mice were raised either in standard or environmentally enriched cages and these mice were then tested for social recognition. WT females in both environmentally...
Show moreAutism Spectrum Disorder (ASD) can be can be caused by numerous different genetic abnormalities, one of which is Pten haploinsufficiency. There is some evidence to suggest that environmental enrichment can decrease the symptoms of ASD and Pten mutant mice have been shown to have altered social behaviors. Therefore, Pten and WT mice were raised either in standard or environmentally enriched cages and these mice were then tested for social recognition. WT females in both environmentally enriched and standard cages and Pten males raised in environmentally enriched cages can recognize and distinguish between other mice. Pten females raised in both standard and environmentally enriched cages, and Pten males in standard cages did not show statistically significant recognition. WT males in both environmentally enriched and standard cages also lacked significant recognition. This outcome indicates that either the experimental protocol should be re-examined or that more mice are required for the experiment.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00012642
Format: Document (PDF)

Title: IDENTIFYING NOVEL GENETIC MODIFIERS OF BRAIN OVERGROWTH IN THE CORTEX OF A MOUSE MODEL OF MACROCEPHALY/AUTISM SYNDROME.
Creator: Cabral, Stacy, Macleod, Gregory, Florida Atlantic University, Harriet L. Wilkes Honors College
Abstract/Description: Phosphatase and tensin homologue (PTEN) is a gene that, when mutated, can cause macrocephaly/autism syndrome. The Pten mutant mouse model will help identify genetic modifiers of Pten-related neurodevelopmental phenotypes, with the goal of gaining insight into the polygenic nature of autism. We hypothesize that genes that display spatiotemporal coexpression patterns similar to Pten in the developing brain are candidates to genetically interact with Pten. Fbxw7, has been identified as a strong...
Show morePhosphatase and tensin homologue (PTEN) is a gene that, when mutated, can cause macrocephaly/autism syndrome. The Pten mutant mouse model will help identify genetic modifiers of Pten-related neurodevelopmental phenotypes, with the goal of gaining insight into the polygenic nature of autism. We hypothesize that genes that display spatiotemporal coexpression patterns similar to Pten in the developing brain are candidates to genetically interact with Pten. Fbxw7, has been identified as a strong candidate. We have conditionally deleted Fbxw7 (Fbxw7 cKO), Pten (Pten cHet), and Pten and Fbxw7 together (Pten and Fbxw7 double mutant) in the developing cerebral cortex. We found Fbxw7 cKO mice have decreased cortical mass and cell number, increased cell density, hydrocephalus and premature lethality. Pten cHet mice display increased cortical mass and cell number, with unchanged cell density and no hydrocephalus or premature lethality. Strikingly, Pten and Fbxw7 double mutant mice had the exact phenocopy of Pten cHet mice, indicating a surprising epistatic interaction between Pten and Fbxw7, in which Pten overrides the effects of Fbxw7. Further work will explore the mechanism of this interaction and will characterize cortical phenotypes in mutant animals.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00012611
Format: Document (PDF)

Title: INHIBITION OF DERMATOPHILUS CONGOLENSIS USING TOPICAL PRODUCTS.
Creator: Miller, Rachel, Macleod, Gregory, Florida Atlantic University, Harriet L. Wilkes Honors College
Abstract/Description: Dermatophilus congolensis is a gram positive, non-acid fast, facultative anaerobic actinomycetes that causes an epidermal skin infection in bovine, ovine, and equine species. This thesis studies the inhibitory effects of common antibacterial topical products on Dermatophilus congolensis. An initial experiment was performed on equine subjects and a secondary experiment was performed using a live strain of the bacteria. Seven different topical products were used in the final experiment, each...
Show moreDermatophilus congolensis is a gram positive, non-acid fast, facultative anaerobic actinomycetes that causes an epidermal skin infection in bovine, ovine, and equine species. This thesis studies the inhibitory effects of common antibacterial topical products on Dermatophilus congolensis. An initial experiment was performed on equine subjects and a secondary experiment was performed using a live strain of the bacteria. Seven different topical products were used in the final experiment, each showing some level of growth inhibition. Chlorhexidine 2% scrub was by far the most potent product with the greatest growth inhibition in each experiment. The use of a topical product such as Chlorhexidine is not only effective, but it helps to reduce bacterial resistance.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00012608
Format: Document (PDF)

Title: The Lack of CuZnSOD Leads to Impaired Neurotransmitter Release, Neuromuscular Junction Destabilization and Reduced Muscle Strength in Mice.
Creator: Shi, Yun, Ivannikov, Maxim V., Walsh, Michael E., Liu, Yuhong, Zhang, Yiqiang, Jaramillo, Carlos A., Macleod, Gregory, Van Remmen, Holly, Phillips, William
Abstract/Description: Elevated reactive oxygen species (ROS) production and ROS-dependent protein damage is a common observation in the pathogenesis of many muscle wasting disorders, including sarcopenia. However, the contribution of elevated ROS levels to –a breakdown in neuromuscular communication and muscle atrophy remains unknown. In this study, we examined a copper zinc superoxide dismutase [CuZnSOD (Sod1)] knockout mouse (Sod1-/-), a mouse model of elevated oxidative stress that exhibits accelerated loss of...
Show moreElevated reactive oxygen species (ROS) production and ROS-dependent protein damage is a common observation in the pathogenesis of many muscle wasting disorders, including sarcopenia. However, the contribution of elevated ROS levels to –a breakdown in neuromuscular communication and muscle atrophy remains unknown. In this study, we examined a copper zinc superoxide dismutase [CuZnSOD (Sod1)] knockout mouse (Sod1-/-), a mouse model of elevated oxidative stress that exhibits accelerated loss of muscle mass, which recapitulates many phenotypes of sarcopenia as early as 5 months of age. We found that young adult Sod1-/- mice display a considerable reduction in hind limb skeletal muscle mass and strength when compared to age-matched wild-type mice. These changes are accompanied by gross alterations in neuromuscular junction (NMJ) morphology, including reduced occupancy of the motor endplates by axons, terminal sprouting and axon thinning and irregular swelling. Surprisingly however, the average density of acetylcholine receptors in endplates is preserved. Using in vivo electromyography and ex vivo electrophysiological studies of hind limb muscles in Sod1-/- mice, we found that motor axons innervating the extensor digitorum longus (EDL) and gastrocnemius muscles release fewer synaptic vesicles upon nerve stimulation. Recordings from individually identified EDL NMJs show that reductions in neurotransmitter release are apparent in the Sod1-/- mice even when endplates are close to fully innervated. However, electrophysiological properties, such as input resistance, resting membrane potential and spontaneous neurotransmitter release kinetics (but not frequency) are similar between EDL muscles of Sod1-/- and wild-type mice. Administration of the potassium channel blocker 3,4-diaminopyridine, which broadens the presynaptic action potential, improves both neurotransmitter release and muscle strength. Together, these results suggest that ROS-associated motor nerve terminal dysfunction is a contributor to the observed muscle changes in Sod1-/- mice.
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Date Issued: 2014-06-27
PURL: http://purl.flvc.org/fau/fd/FAUIR000036
Format: Citation

Title: A Framework for Understanding Power Supply and Demand in Presynaptic Nerve Terminals.
Creator: Justs, Karlis Anthony, Macleod, Gregory T., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: The molecular mechanisms of synaptic function and development have been studied extensively, but little is known about the energy requirements of synapses, or the mechanisms that coordinate their energy production with their metabolic demands. These are oversights, as synapses with high energy demands are more susceptible to degeneration and degrade in the early stages of diseases such as amyotrophic lateral sclerosis, spinal muscle atrophy and Parkinson’s disease. Here, in a structure...
Show moreThe molecular mechanisms of synaptic function and development have been studied extensively, but little is known about the energy requirements of synapses, or the mechanisms that coordinate their energy production with their metabolic demands. These are oversights, as synapses with high energy demands are more susceptible to degeneration and degrade in the early stages of diseases such as amyotrophic lateral sclerosis, spinal muscle atrophy and Parkinson’s disease. Here, in a structure-function study at Drosophila motor neuron terminals, a neurophysiological model was generated to investigate how power (ATP/s) supply is integrated to satisfy the power demand of presynaptic terminals. Power demands were estimated from six nerve terminals through direct measurements of neurotransmitter release and Ca2+ entry, as well as theoretical estimation of Na+ entry and power demands at rest (cost of housekeeping). The data was leveraged with a computational model that simulated the power demands of the terminals during their physiological activity, revealing high volatility in which power demands can increase 15-fold within milliseconds as neurons transition from rest to activity. Another computational model was generated that simulated ATP production scenarios regarding feedback to the power supply machinery (Oxphos and glycolysis) through changes in nucleotide concentrations, showing that feedback from nucleotides alone fail to stimulate power supply to match the power demands of each terminal. Failure of feedback models invokes the need for feed forward mechanisms (such as Ca2+) to stimulate power supply machinery to match power demands. We also quantified mitochondrial volume, density, number and size in each nerve terminal, revealing all four features positively correlate with the terminals power demands. This suggests the terminals enhance their oxidative capacity by increasing mitochondrial content to satisfy their power demands. And lastly, we demonstrate that abolishing an ATP buffering system (the phosphagen system) does not impair neurotransmission in the nerve terminals, suggesting motor nerve terminals are capable of satisfying their power demands without the ATP buffering system.
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Date Issued: 2019
PURL: http://purl.flvc.org/fau/fd/FA00013323
Subject Headings: Presynaptic Terminals, Adenosine triphosphate, Synapses--metabolism, Bioenergetics
Format: Document (PDF)

Title: Presynaptic Determinants of Synaptic Strength and Energy Efficiency at Drosophila Neuromuscular Junctions.
Creator: Lu, Zhongmin, Macleod, Gregory, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Changes in synaptic strength underlie synaptic plasticity, the cellular substrate for learning and memory. Disruptions in the mechanisms that regulate synaptic strength closely link to many developmental, neurodegenerative and neurological disorders. Release site probability (PAZ) and active zone number (N) are two important presynaptic determinants of synaptic strength; yet, little is known about the processes that establish the balance between N and PAZ at any synapse. Furthermore, it is...
Show moreChanges in synaptic strength underlie synaptic plasticity, the cellular substrate for learning and memory. Disruptions in the mechanisms that regulate synaptic strength closely link to many developmental, neurodegenerative and neurological disorders. Release site probability (PAZ) and active zone number (N) are two important presynaptic determinants of synaptic strength; yet, little is known about the processes that establish the balance between N and PAZ at any synapse. Furthermore, it is not known how PAZ and N are rebalanced during synaptic homeostasis to accomplish circuit stability. To address this knowledge gap, we adapted a neurophysiological experimental system consisting of two functionally differentiated glutamatergic motor neurons (MNs) innervating the same target. Average PAZ varied between nerve terminals, motivating us to explore benefits for high and low PAZ, respectively. We speculated that high PAZ confers high-energy efficiency. To test the hypothesis, electrophysiological and ultrastructural measurements were made. The terminal with the highest PAZ released more neurotransmitter but it did so with the least total energetic cost. An analytical model was built to further explore functional and structural aspects in optimizing energy efficiency. The model supported that energy efficiency optimization requires high PAZ. However, terminals with low PAZ were better able to sustain neurotransmitter release. We suggest that tension between energy efficiency and stamina sets PAZ and thus determines synaptic strength. To test the hypothesis that nerve terminals regulate PAZ rather than N to maintain synaptic strength, we induced sustained synaptic homeostasis at the nerve terminals. Ca2+ imaging revealed that terminals of the MN innervating only one muscle fiber utilized greater Ca2+ influx to achieve compensatory neurotransmitter release. In contrast, morphological measurements revealed that terminals of the MN inner vating multiple postsynaptic targets utilized an increase in N to achieve compensatory neurotransmitter release, but this only occurred at the terminal of the affected postsynaptic target. In conclusion, this dissertation provides several novel insights into a prominent question in neuroscience: how is synaptic strength established and maintained. The work indicates that tension exists between energy efficiency and stamina in neurotransmitter release likely influences PAZ. Furthermore, PAZ and N are rebalanced differently between terminals during synaptic homeostasis.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004519, http://purl.flvc.org/fau/fd/FA00004519
Subject Headings: Drosophila melanogaster--Nervous system., Drosophila melanogaster--Cytogenetics., Fruit-flies--Development., Fruit-flies--Nervous system., Genetic transcription., Transcription factors., Cellular signal transduction., Cellular control mechanisms., Myoneural junction.
Format: Document (PDF)

Title: pH Dynamics within the Drosophila Synaptic Cleft During Activity.
Creator: Feghhi, Touhid, Lau, Andy W.C., Macleod, Gregory T., Florida Atlantic University, Department of Physics, Charles E. Schmidt College of Science
Abstract/Description: Acute pH sensitivity of many neural mechanisms highlights the vulnerability of neurotransmission to the pH of the extracellular milieu. The dogma is that the synaptic cleft will acidify upon neurotransmission because the synaptic vesicles corelease neurotransmitters and protons to the cleft, and the direct data from sensory ribbon-type synapses support the acidification of the cleft. However, ribbon synapses have a much higher release probability than conventional synapses, and it’s not...
Show moreAcute pH sensitivity of many neural mechanisms highlights the vulnerability of neurotransmission to the pH of the extracellular milieu. The dogma is that the synaptic cleft will acidify upon neurotransmission because the synaptic vesicles corelease neurotransmitters and protons to the cleft, and the direct data from sensory ribbon-type synapses support the acidification of the cleft. However, ribbon synapses have a much higher release probability than conventional synapses, and it’s not established whether conventional synapses acidify as well. To test the acidification of the cleft in the conventional synapse, we used genetically encoded fluorescent pH reporters targeted to the synaptic cleft of Drosophila larvae. We observed alkalinization rather than acidification during activity, and this alkalinization was dependent on the exchange of protons for calcium at the postsynaptic membrane. A reaction-diffusion computational model of the pH dynamics at the Drosophila larval neuromuscular junction was developed to leverage the experimental data. The model incorporates the release of glutamate, ATP, and protons from synaptic vesicles into the cleft, PMCA activity, bicarbonate, and phosphate buffering systems. By means of numerical simulations, we reveal a highly dynamic pH landscape within the synaptic cleft, harboring deep but exceedingly rapid acid transients that give way to a prolonged period of alkalinization.
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Date Issued: 2023
PURL: http://purl.flvc.org/fau/fd/FA00014221
Subject Headings: Synapses, pH (Chemistry), Hydrogen-ion concentration., Synaptic Transmission, Drosophila
Format: Document (PDF)

Title: The Dynamic pH Landscape At The Drosophila NMJ Synaptic Cleft And Its Implication In Neurotransmission.
Creator: Hernandez, Roberto X., Macleod, Gregory T., Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
Abstract/Description: The intricate processes governing cellular pH and its impact on protein and cellular function have been extensively explored. However, our understanding of the pH fluctuations that occur during routine cellular activities and their potential to modulate cell function remains, particularly within the highly dynamic pH landscape of a synapse. Investigating the scale, directionality, and temporal characteristics of these activity-dependent pH fluctuations at synapses is of paramount interest, as...
Show moreThe intricate processes governing cellular pH and its impact on protein and cellular function have been extensively explored. However, our understanding of the pH fluctuations that occur during routine cellular activities and their potential to modulate cell function remains, particularly within the highly dynamic pH landscape of a synapse. Investigating the scale, directionality, and temporal characteristics of these activity-dependent pH fluctuations at synapses is of paramount interest, as it carries profound implications for neurotransmitter release and signal transduction. Employing both empirical and computational modeling methods, our research explores the dynamic pH environment within the synaptic cleft of Drosophila glutamatergic motor neuron Ib terminals during synaptic activity and reveals its significance in modulating neurotransmission. Contrary to popular belief, we discovered that these terminals undergo activity-dependent extracellular alkalinization in response to both single action potentials and burst stimulation. This surprising phenomenon was also observed at the mouse calyx of Held. We found activity-dependent alkalinization to be predominantly driven by Ca2+ movement across the postsynaptic membrane, and by targeting pH indicators to subcellular domains, we identified alkalinization to primarily occur within the cleft.
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Date Issued: 2023
PURL: http://purl.flvc.org/fau/fd/FA00014346
Subject Headings: Neurotransmission, Drosophila, Hydrogen-Ion Concentration, Motor Neurons, Optogenetics
Format: Document (PDF)

Title: Neuronal Energetics: Mitochondrial Distribution and The Phosphagen System.
Creator: Riboul, Danielle V., Macleod, Gregory T., Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
Abstract/Description: The relationship between neuronal function and energy metabolism is a field of intense inquiry and while bioenergetic per se are well understood, we lack a good understanding of the ways in which these mechanisms overcome the challenges presented by the unique morphology of neurons and their volatile energy demands. Here we examined the extent to which these challenges can be met through strategic mitochondrial placement and the support of a phosphagen system. We examined fluctuations in...
Show moreThe relationship between neuronal function and energy metabolism is a field of intense inquiry and while bioenergetic per se are well understood, we lack a good understanding of the ways in which these mechanisms overcome the challenges presented by the unique morphology of neurons and their volatile energy demands. Here we examined the extent to which these challenges can be met through strategic mitochondrial placement and the support of a phosphagen system. We examined fluctuations in energy demand of Drosophila larval motor neurons utilizing a combination of computational modeling and empirical analysis, and uncovered a neglected aspect of cellular energy metabolism that appears to accommodate the stress of highly volatile energy demands. Our findings highlight a reliance on the phosphagen system to buffer against rapid changes in the rate of ATP consumption induced by burst firing. The knockdown of a key element in the phosphagen system of invertebrates, arginine kinase, revealed a suppression of the mitochondrial proton motive force, and a more rapid decline in the presynaptic ATP/ADP ratio during burst firing. The knock down of arginine kinase also revealed metabolic shifts that indicated a compensatory increase in glycolysis, but, surprisingly, few consequences for either presynaptic Ca2+ handling or neurotransmission. In a final effort to ensure that we were imposing a metabolic load adequate to challenge these motor neurons, we developed an ex vivo calcium clearance assay and in vivo locomotor performance assay – currently in their final stages of validation.
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Date Issued: 2024
PURL: http://purl.flvc.org/fau/fd/FA00014419
Subject Headings: Mitochondria, Neurons, Energy metabolism
Format: Document (PDF)

Honors Student Theses (6)	+ -
FAU Theses and Dissertations (5)	+ -
FAU College Collections (1)	+ -
FAU Undergraduate Student Research (1)	+ -

Drosophila (2)	+ -
Adenosine triphosphate (1)	+ -
Bioenergetics (1)	+ -
Cellular control mechanisms. (1)	+ -
Cellular signal transduction. (1)	+ -

College students --Research --United States. (1)	+ -
Drosophila melanogaster--Cytogenetics. (1)	+ -
Drosophila melanogaster--Nervous system. (1)	+ -
Energy metabolism (1)	+ -
Fruit-flies--Development. (1)	+ -
Fruit-flies--Nervous system. (1)	+ -
Genetic transcription. (1)	+ -
Hydrogen-Ion Concentration (1)	+ -
Hydrogen-ion concentration. (1)	+ -
Mitochondria (1)	+ -
Motor Neurons (1)	+ -
Myoneural junction. (1)	+ -
Neurons (1)	+ -
Neurotransmission (1)	+ -
Optogenetics (1)	+ -
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article (1)	+ -
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Harriet L. Wilkes Honors College (7)	+ -
Charles E. Schmidt College of Science (5)	+ -
Department of Biological Sciences (4)	+ -

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