subject:(Other Neuroscience AND Neurobiology)

University of Iowa

1. Yin, Terry. Neuroprotective strategies for traumatic brain injury.

Degree: PhD, Molecular Psychiatry, 2015, University of Iowa

► Traumatic brain injury (TBI) causes life-debilitating conditions. While patient survival after a TBI has improved, the outlook for quality of life after TBI currently… (more)

▼ Traumatic brain injury (TBI) causes life-debilitating conditions. While patient survival after a TBI has improved, the outlook for quality of life after TBI currently remains poor. In order to address this problem, there is a significant unmet need for new therapeutic options to prevent progression of deficits associated with TBI. To this end, we investigated two strategies to combat the deleterious affect of TBI. First, we targeted cerebral acidosis associated with TBI by testing whether disruption of acid sensing ion channel 1a (ASIC1a) in CNS, or buffering acidosis with sodium bicarbonate, could prevent neurological deficits after TBI. We next tested whether treatment with the neovel class of aminopropyl carbozoles, known as the P7C3 series, could also prevent TBI-associated neurological decline. Using the mouse fluid percussion injury model of TBI, we observed post-injury acidosis in the cortex, consistent with what has been shown in humans following brain injury. Administering HCO3- after fluid percussion injury prevented acidosis and reduced neurodegeneration. Because acidosis activates acid sensing ion channels (ASICs), we also studied AIC1a-/- mice and found reduced neurodegeneration after injury. Both HCO3-3 administration and loss of ASIC1a reduced functional deficits caused by fluid percussion injury. These results suggest that fluid percussion injury induces cerebral acidosis, which activates ASIC channels in the brain and contributes to neurodegeneration. Blocking ASIC1aactivity may thus offer a new therapeutic strategy to attenuate the adverse consequences of TBI. We next applied the blast injury model of TBI to test whether the P7C3 class of neuroprotective aminopropyl carbazoles would be of therapeutic benefit. In addition to preventing neuronal cell death, P7C3 molecules also preserved axonal integrity before neuronal cell loss in this model. The mechanism of P7C3 neuroprotection may be linked to its ability to activate the enzyme, nicotinamide phosphoribosyltransferase, which catalyzed the rate limiting step of nicotinamide adenine dinucleotide salvage pathway. Administration of the lead compound in the series, P7C3-S243, 1 day after blast-mediated TBI blocked axonal degeneration and preserved normal synaptic activity. P7C3-S243 administration also reduced neuronal functional deficits, including impaired learning, memory, and motor coordination in mice. We additionally reported persistent neurologic deficits and acquisition of anxiety-like phenotype in untreated animals 8-months after blast-mediated TBI. Optimized variants of P7C3 thus offer hope for identifying neuroprotective agents for conditions involving axonal damage, neuronal cell death, or both. Together, the results of this body of work identify novel therapeutic interventions that may attenuate deficits associated with TBI, and thus improve the quality of life in people after TBI. Advisors/Committee Members: Pieper, Andrew A. (supervisor).

Subjects/Keywords: Neuroscience and Neurobiology; Other Psychiatry and Psychology

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APA (6^th Edition):

Yin, T. (2015). Neuroprotective strategies for traumatic brain injury. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1811

Chicago Manual of Style (16^th Edition):

Yin, Terry. “Neuroprotective strategies for traumatic brain injury.” 2015. Doctoral Dissertation, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/1811.

MLA Handbook (7^th Edition):

Yin, Terry. “Neuroprotective strategies for traumatic brain injury.” 2015. Web. 07 Mar 2021.

Vancouver:

Yin T. Neuroprotective strategies for traumatic brain injury. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/1811.

Council of Science Editors:

Yin T. Neuroprotective strategies for traumatic brain injury. [Doctoral Dissertation]. University of Iowa; 2015. Available from: https://ir.uiowa.edu/etd/1811

West Virginia University

2. Dillon-Seeger, Danielle Leigh. Discrimination and behavioral responses to communication signals compared across Apteronotids.

Degree: MS, Biology, 2019, West Virginia University

URL: https://doi.org/10.33915/etd.7392 ; https://researchrepository.wvu.edu/etd/7392

► Sensory systems are often uniquely tailored to encode behaviorally relevant signals and comparative studies across species can thus reveal how evolutionary changes shape sensory… (more)

Subjects/Keywords: Chirps; Communication; Behavior; Electroreception; Perception.; Behavioral Neurobiology; Other Neuroscience and Neurobiology

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APA (6^th Edition):

Dillon-Seeger, D. L. (2019). Discrimination and behavioral responses to communication signals compared across Apteronotids. (Thesis). West Virginia University. Retrieved from https://doi.org/10.33915/etd.7392 ; https://researchrepository.wvu.edu/etd/7392

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dillon-Seeger, Danielle Leigh. “Discrimination and behavioral responses to communication signals compared across Apteronotids.” 2019. Thesis, West Virginia University. Accessed March 07, 2021. https://doi.org/10.33915/etd.7392 ; https://researchrepository.wvu.edu/etd/7392.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dillon-Seeger, Danielle Leigh. “Discrimination and behavioral responses to communication signals compared across Apteronotids.” 2019. Web. 07 Mar 2021.

Vancouver:

Dillon-Seeger DL. Discrimination and behavioral responses to communication signals compared across Apteronotids. [Internet] [Thesis]. West Virginia University; 2019. [cited 2021 Mar 07]. Available from: https://doi.org/10.33915/etd.7392 ; https://researchrepository.wvu.edu/etd/7392.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dillon-Seeger DL. Discrimination and behavioral responses to communication signals compared across Apteronotids. [Thesis]. West Virginia University; 2019. Available from: https://doi.org/10.33915/etd.7392 ; https://researchrepository.wvu.edu/etd/7392

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Wilfrid Laurier University

3. Katzman, Hailey. The Effects of Dorsal Lateral Telencephalon Lesions on Zebrafish Social Behaviour.

Degree: 2020, Wilfrid Laurier University

URL: https://scholars.wlu.ca/etd/2243

► Zebrafish are extremely social and aggregate in groups to form shoals. This social behaviour has been studied in the wild and in a laboratory setting,… (more)

Subjects/Keywords: Neuroscience; Psychology; Behaviour; Zebrafish; Social behaviour; Cognition; Other Neuroscience and Neurobiology

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APA (6^th Edition):

Katzman, H. (2020). The Effects of Dorsal Lateral Telencephalon Lesions on Zebrafish Social Behaviour. (Thesis). Wilfrid Laurier University. Retrieved from https://scholars.wlu.ca/etd/2243

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Katzman, Hailey. “The Effects of Dorsal Lateral Telencephalon Lesions on Zebrafish Social Behaviour.” 2020. Thesis, Wilfrid Laurier University. Accessed March 07, 2021. https://scholars.wlu.ca/etd/2243.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Katzman, Hailey. “The Effects of Dorsal Lateral Telencephalon Lesions on Zebrafish Social Behaviour.” 2020. Web. 07 Mar 2021.

Vancouver:

Katzman H. The Effects of Dorsal Lateral Telencephalon Lesions on Zebrafish Social Behaviour. [Internet] [Thesis]. Wilfrid Laurier University; 2020. [cited 2021 Mar 07]. Available from: https://scholars.wlu.ca/etd/2243.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Katzman H. The Effects of Dorsal Lateral Telencephalon Lesions on Zebrafish Social Behaviour. [Thesis]. Wilfrid Laurier University; 2020. Available from: https://scholars.wlu.ca/etd/2243

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas Medical Center

4. Eagleman, Sarah, Ph.D. EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING.

Degree: PhD, 2014, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/432

► Psychophysical experiments in humans have demonstrated that improvements in perceptual learning tasks occur following daytime rests. The neural correlates of how rest influences subsequent… (more)

▼ Psychophysical experiments in humans have demonstrated that improvements in perceptual learning tasks occur following daytime rests. The neural correlates of how rest influences subsequent sensory processing during these tasks remain unclear. One possible neural mechanism that may underlie this behavioral improvement is reactivation. Previously evoked network activity reoccurs – reactivates - in the absence of further stimulation. Reactivation was initially discovered in the hippocampus but has now been found in several brain areas including cortex. This phenomenon has been implicated as a general mechanism by which neural networks learn and store sensory information. However, whether reactivation occurs in areas relevant for perceptual learning is unknown. To investigate how sleep affects perceptual learning at the level of single neurons and networks, an experimental paradigm was designed to simultaneously perform extracellular recordings in visual cortical area V4 along with sleep classification in monkeys. V4 is a midlevel visual area that responds to shapes, textures, and colors. Additionally, V4 is important for perceptual learning and shows significant attentional effects. In this experiment, two monkeys were trained to perform a delayed match-to-sample task before and after a 20 minute rest in a dark, quiet room. Whether monkeys exhibit the same improvements in perceptual learning previously shown in humans is unknown. Here, monkeys did improve task performance following the 20 minute rest. Additionally, whether neural networks in V4 could reactivate was explored in a passive fixation task. A reactivation of previously evoked sequential activity was observed in V4 networks following stimulus exposure in the absence of visual stimulation. This reactivation was time-locked to when the stimulus was expected to occur after a cue, which indicated to monkeys the trial was starting. Finally, whether the delayed match-to-sample task-evoked activity was spontaneously reactivated during the 20 minute rest period was tested. No evidence to suggest that reactivation occurs during this time was observed. Considering previous reactivation results, this suggests the cue is necessary to initiate the reactivation. In summary, this work represents an investigation of the neural correlates that underlie behavioral performance improvements following daytime rest. Results can provide a better understanding of how daytime naps improve perceptual learning. Advisors/Committee Members: Valentin Dragoi, Ph.D., Daniel Felleman, Ph.D., William Seifert, Ph.D..

Subjects/Keywords: electrophysiology; visual cortex; sleep; reactivation; replay; Cognitive Neuroscience; Other Neuroscience and Neurobiology; Systems Neuroscience

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APA (6^th Edition):

Eagleman, Sarah, P. D. (2014). EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/432

Chicago Manual of Style (16^th Edition):

Eagleman, Sarah, Ph D. “EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING.” 2014. Doctoral Dissertation, Texas Medical Center. Accessed March 07, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/432.

MLA Handbook (7^th Edition):

Eagleman, Sarah, Ph D. “EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING.” 2014. Web. 07 Mar 2021.

Vancouver:

Eagleman, Sarah PD. EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING. [Internet] [Doctoral dissertation]. Texas Medical Center; 2014. [cited 2021 Mar 07]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/432.

Council of Science Editors:

Eagleman, Sarah PD. EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING. [Doctoral Dissertation]. Texas Medical Center; 2014. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/432

5. Mondo, Erica. Investigating Microglia-Vascular Interactions in the Developing and Adult Central Nervous System.

Degree: Neuroscience, Neurobiology; Schafer Lab, 2020, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/1105

► Microglia, the resident macrophages of the central nervous system (CNS), are dynamic cells, constantly extending and retracting their processes as they contact and functionally… (more)

▼ Microglia, the resident macrophages of the central nervous system (CNS), are dynamic cells, constantly extending and retracting their processes as they contact and functionally regulate neurons and other glial cells. There is far less known about how microglia interact with the CNS vasculature, particularly under healthy steady-state conditions. Here, I provide the first extensive characterization of juxtavascular microglia in the healthy, postnatal brain and identify a molecular mechanism regulating the timing of these interactions during development. Using the mouse cerebral cortex, I show that microglia are intimately associated with the vasculature in the CNS, directly contacting the basal lamina in vascular sites that are devoid of astrocyte endfeet. I demonstrate a high percentage of microglia are associated with the vasculature during the first week of postnatal development, which is concomitant with a peak in microglial colonization of the cortex and recruitment to synapses. I find that as microglia colonize the cortex, juxtavascular microglia are highly motile along vessels and become largely stationary as the brain matures. 2-photon live imaging in adult mice reveals that these vascular-associated microglia in the mature brain are stable and stationary for several weeks. Further, a decrease in microglia motility along the vasculature is tightly correlated with the expansion of astrocyte endfeet along the vasculature. Finally, I provide evidence that the timing of these microglia-vascular interactions during development is regulated by the microglial fractalkine receptor (CX3CR1). Together, these data support a model by which microglia use the vasculature as a scaffold to migrate and colonize the developing brain and the timing of these associations is modulated by CX3CR1. This migration along the vasculature becomes restricted as astrocyte vascular endfoot territory expands and, upon maturation, vascular-associated microglia become largely stationary. Advisors/Committee Members: Dorothy Schafer.

Subjects/Keywords: Microglia; Blood Vessel; Development; Fractalkine Receptor; Other Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mondo, E. (2020). Investigating Microglia-Vascular Interactions in the Developing and Adult Central Nervous System. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/1105

Chicago Manual of Style (16^th Edition):

Mondo, Erica. “Investigating Microglia-Vascular Interactions in the Developing and Adult Central Nervous System.” 2020. Doctoral Dissertation, U of Massachusetts : Med. Accessed March 07, 2021. https://escholarship.umassmed.edu/gsbs_diss/1105.

MLA Handbook (7^th Edition):

Mondo, Erica. “Investigating Microglia-Vascular Interactions in the Developing and Adult Central Nervous System.” 2020. Web. 07 Mar 2021.

Vancouver:

Mondo E. Investigating Microglia-Vascular Interactions in the Developing and Adult Central Nervous System. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2020. [cited 2021 Mar 07]. Available from: https://escholarship.umassmed.edu/gsbs_diss/1105.

Council of Science Editors:

Mondo E. Investigating Microglia-Vascular Interactions in the Developing and Adult Central Nervous System. [Doctoral Dissertation]. U of Massachusetts : Med; 2020. Available from: https://escholarship.umassmed.edu/gsbs_diss/1105

University of South Florida

6. Tetlow, Amber M. Evaluation of Aging and Genetic Mutation Variants on Tauopathy.

Degree: 2020, University of South Florida

URL: https://scholarcommons.usf.edu/etd/8596

► Alzheimer’s disease (AD) is characterized by amyloid β plaques and neurofibrillary tau tangles (NFTs). While research has demonstrated amyloid pathology occurs prior to tau pathology,… (more)

▼ Alzheimer’s disease (AD) is characterized by amyloid β plaques and neurofibrillary tau tangles (NFTs). While research has demonstrated amyloid pathology occurs prior to tau pathology, or tauopathy, tau has proven to be more toxic. Tauopathy is associated with cognitive declines and neurodegeneration. These findings have highlighted the importance of further understanding tauopathy. In the progression of tauopathy, there is an observable immune response that can be measured by glial cells such as microglia. Activated microglia are known to exacerbate tauopathy rather than reducing the pathology. Research has indicated that with increased age there is an increased risk for AD-related tauopathy and a more reactive, or primed immune response. Therefore, it is important to further understand how tauopathy and immune markers change in respect to age to potentially identify critical periods that might be advantageous for future interventions. This dissertation is aimed at understanding the effects of age and genetic mutant variants of tau in different animal models of tauopathy over three different studies. In study one, a commonly used transgenic model of tauopathy, rTg4510, was studied to examine how markers of tauopathy and tauopathy-related pathology differ over the life course. Regression analyses were conducted to determine the best models of fit (linear vs non-linear models of fit) for each marker. Results indicated that not all the markers of pathology in this model progress at the same rate or in the same manner. However, there was an overall increase in pathological events with increased age; especially in histological sections and the detergent insoluble homogenate fraction that contains pathological aggregates. In study two, age differences between young, middle-aged, and old animals that received either AAV9 GFP or AAV9 tauP301L intracranial injections were examined. Two-way ANOVAs and two-way repeated measures ANOVAs were conducted to determine group differences on measures of tauopathy, tauopathy-related markers of pathology including immune activation and neurodegeneration, and behavioral assessments of motor and cognitive impairments. These results indicated the old mice had higher levels of early phosphorylated tau, neurofibrillary tau tangles (NFTs), and reactive immune activation. Behavioral assessments evidenced a reduction in performance in the old animals irrespective of the injection group. However, only the younger GFP injected mice (young and middle-aged) were able to demonstrate mastery of the memory task. The old GFP and tauP301L injected mice were not able to achieve the historical learning criterion in the memory task. In study three, viral constructs expressing different tau variants were employed including, AAV9 tauP301L, AAV9 tauR406W, AAV9 tauwild-type, and AAV9 GFP intracranial injections were conducted in middle-aged mice to identify whether tau mutations associated with human disease could produce a translational model of tauopathy. One-way ANOVAs and one-way repeated measures ANOVAs…

Subjects/Keywords: Alzheimer's disease; gerontology; neurobiology; neuroscience; tau; Neurosciences; Other Medical Specialties

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APA (6^th Edition):

Tetlow, A. M. (2020). Evaluation of Aging and Genetic Mutation Variants on Tauopathy. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/8596

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tetlow, Amber M. “Evaluation of Aging and Genetic Mutation Variants on Tauopathy.” 2020. Thesis, University of South Florida. Accessed March 07, 2021. https://scholarcommons.usf.edu/etd/8596.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tetlow, Amber M. “Evaluation of Aging and Genetic Mutation Variants on Tauopathy.” 2020. Web. 07 Mar 2021.

Vancouver:

Tetlow AM. Evaluation of Aging and Genetic Mutation Variants on Tauopathy. [Internet] [Thesis]. University of South Florida; 2020. [cited 2021 Mar 07]. Available from: https://scholarcommons.usf.edu/etd/8596.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tetlow AM. Evaluation of Aging and Genetic Mutation Variants on Tauopathy. [Thesis]. University of South Florida; 2020. Available from: https://scholarcommons.usf.edu/etd/8596

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas Medical Center

7. Robinson, Caleb R. Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy.

Degree: PhD, 2014, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/485

► Bortezomib is a proteasome inhibitor used in the treatment of multiple myeloma and other non-solid malignancies, alone or in combination with other chemotherapy drugs.… (more)

▼ Bortezomib is a proteasome inhibitor used in the treatment of multiple myeloma and other non-solid malignancies, alone or in combination with other chemotherapy drugs. Like other chemotherapeutic agents, bortezomib treatment is frequently accompanied by chemotherapy-induced peripheral neuropathy (CIPN) that may be dose-limiting, adversely affecting quality of life and prognosis. The mechanisms behind bortezomib-induced peripheral neuropathy (BIPN) and CIPN overall are largely unknown. Recent findings in other pain models have indicated substantial involvement of glial cells in chronic pain. Although injury models have shown activation of both astrocytes and microglia following insult, research in other CIPN models has shown astrocytic activation in the absence of microglial activation. The central hypothesis of this dissertation is that the activity of astrocytes is correlated with behavioral changes observed in a rat model of BIPN in a manner that may directly contribute to these changes in behavior. To investigate this, the work of this dissertation 1) established the multimodal changes to behavior and showed increases in spinal neuron firing in BIPN, 2) quantified activity of astrocytes and whether changes were prevented by minocycline, an anti-inflammatory drug that vi prevents glial activation, and 3) quantified changes in connexin 43, GLT-1, and GLAST to assess whether astrocytic glutamate transport may be altered in BIPN. The results observed in the first aim were that the rat BIPN model is characterized by selective mechanical hypersensitivity and a significant increase in wide dynamic range (WDR) neuron firing rates and after-discharges. In the second aim, astrocytes in the BIPN model were activated in a manner that paralleled the behavioral changes. Animals co-treated with minocycline resembled saline-treated animals in both astrocytic activation and behaviors. The results in the third aim were that astrocytic gap junctions were increased and GLAST expression was decreased at the height of mechanical sensitivity. Minocycline-treated animals resembled saline-treated animals in expression of these proteins, as well. The overall conclusion was that astrocyte activity closely paralleled behaviors in the BIPN model in a manner that may be explained by their role in glutamate trafficking. Advisors/Committee Members: Patrick M. Dougherty, Ph.D., Edgar T. Walters, Ph.D., Carmen W. Dessauer, Ph.D..

Subjects/Keywords: bortezomib; astrocyte; CIPN; chemotherapy-induced peripheral neuropathy; Medicine and Health Sciences; Nervous System Diseases; Neuroscience and Neurobiology; Other Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robinson, C. R. (2014). Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/485

Chicago Manual of Style (16^th Edition):

Robinson, Caleb R. “Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy.” 2014. Doctoral Dissertation, Texas Medical Center. Accessed March 07, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/485.

MLA Handbook (7^th Edition):

Robinson, Caleb R. “Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy.” 2014. Web. 07 Mar 2021.

Vancouver:

Robinson CR. Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy. [Internet] [Doctoral dissertation]. Texas Medical Center; 2014. [cited 2021 Mar 07]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/485.

Council of Science Editors:

Robinson CR. Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy. [Doctoral Dissertation]. Texas Medical Center; 2014. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/485

University of Kentucky

8. Sethi, Mansi. SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE.

Degree: 2016, University of Kentucky

URL: https://uknowledge.uky.edu/biology_etds/38

► Sleep is a process essential for the well-being of an animal and in humans as much as one-third of our life is spent in sleep.… (more)

▼ Sleep is a process essential for the well-being of an animal and in humans as much as one-third of our life is spent in sleep. Yet, the biological need for sleep still remains a conundrum. Our knowledge of the genes influencing sleep and the mechanisms regulating the process can be advanced with the utilization of genetic and genomic approaches which, in turn, may inform us about the functions of sleep as well. With this goal, I have investigated and examined sleep-wake phenotypes for a variety of transgenic and knock out animals. For the first part of my research (Chapter 3), I examined mouse models of Alzheimer’s disease, and a combined model of Alzheimer’s disease (AD) and Diabetes. Sleep disturbances in case of AD are evident long before the onset of cognitive decline. I investigated sleep-wake alterations in 5XFAD, a double transgenic mouse model of AD which displays an early onset of AD pathology and cognitive impairments. We found that these mice have shorter bout lengths under baseline conditions. This was true for both sexes, however, the effect was more prominent in females. Additionally, females also had a shorter duration of sleep compared to control animals. These overall bout length reductions are indicative of increased sleep fragmentation similar to the ones seen in human AD patients. Inadequate sleep is associated with increased risk for metabolic disorders such as diabetes besides neurodegenerative diseases such as AD. There is also growing evidence that type 2 diabetes mellitus (T2DM) poses an increased risk of AD. To understand how the two conditions interact, we studied a combined mouse model of AD and diabetes (db/AD) which was generated by crossing of db/db (diabetic obese mice) and APP-PS1 (knock-in AD mouse model). The resulting mice showed profound cerebrovascular as well as AD pathology. Both females and males, diabetic AD animals had longer sleep duration compared to non-diabetic AD animals. They also exhibited attenuated sleep-wake rhythms. Females were found to have shorter sleep bouts than males. In addition, significant two way interactions were found for the age and db/AD genotype. Our findings suggest that db genotype and not cerebrovascular pathologies affect sleep in our mouse model. For the last part of my research, we analyzed over 300 single gene knock out mouse lines generated on a C57BL6/NJ background, monitored at The Jackson Laboratory. With this unbiased approach where the knockouts were chosen at random, we identified 55 novel genes affecting various sleep traits, utilizing a variety of statistical approaches. Sex differences were found for a number of knockouts as well as controls. Control females were found to have shorter bout lengths and less sleep duration compared to male littermates.

Subjects/Keywords: amyloid beta; sleep fragmentation; diabetes; phenotyping; piezoelectric system; knockout mice; Behavioral Neurobiology; Molecular and Cellular Neuroscience; Other Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sethi, M. (2016). SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/biology_etds/38

Chicago Manual of Style (16^th Edition):

Sethi, Mansi. “SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE.” 2016. Doctoral Dissertation, University of Kentucky. Accessed March 07, 2021. https://uknowledge.uky.edu/biology_etds/38.

MLA Handbook (7^th Edition):

Sethi, Mansi. “SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE.” 2016. Web. 07 Mar 2021.

Vancouver:

Sethi M. SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE. [Internet] [Doctoral dissertation]. University of Kentucky; 2016. [cited 2021 Mar 07]. Available from: https://uknowledge.uky.edu/biology_etds/38.

Council of Science Editors:

Sethi M. SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE. [Doctoral Dissertation]. University of Kentucky; 2016. Available from: https://uknowledge.uky.edu/biology_etds/38

Wilfrid Laurier University

9. Compton, Chris. The fatigue-associated changes in estimates of persistent inward current in human motor neurons.

Degree: 2018, Wilfrid Laurier University

URL: https://scholars.wlu.ca/etd/2082

► Neuromuscular fatigue is associated with reduced supraspinal drive. Similarly, intracortical facilitation and muscle activation are reduced following concussion. Both fatigue and mild traumatic brain injury… (more)

▼ Neuromuscular fatigue is associated with reduced supraspinal drive. Similarly, intracortical facilitation and muscle activation are reduced following concussion. Both fatigue and mild traumatic brain injury are associated with increased noradrenergic and serotonergic activity in animal models. Given that monoaminergic-dependent persistent inward currents (PIC) set spinal motor neuron (MN) gain, we speculate that PIC will increase during fatigue to compensate for supraspinal hypoexcitability and that this will be more pronounced in people with concussion. Therefore, the purpose of this experiment was to assess spinal MN excitability during fatigue in people with concussion and healthy controls. 20 participants (10 concussion, average age 22.05 ± 2.25) completed two experimental sessions on two separate days (fatigue and rest, randomized and counterbalanced). On the fatigue day, paired motor unit analysis was used to estimate soleus motor neuron PIC, before, during, and after an isometric plantarflexion fatigue protocol (5 sets of 40, 3s ankle plantarflexion contractions at 50% of maximal voluntary contraction). Excitability of the soleus motor neuron pool was assessed at rest using slopes of the H reflex recruitment curve before and after the protocol. On the rest day, estimates of PIC and H reflexes were made at the same time points, but the fatiguing contractions were omitted. Soleus motor neuron PIC and resting H reflexes in people with concussion were not different from the controls at any time point. When the groups were collapsed, maximum voluntary torque declined to 92.63±8.67% (prd (pth (p=0.026) set of fatiguing contractions, returning to baseline by the end of the fatigue protocol (p=0.562). The slopes of the H reflex recruitment curves did not change. It is likely that increased monoaminergic drive seen during exercise activates soleus motor neuron PIC to enhance motor output. The increased gain provided by PICs may serve to enhance motor output during fatiguing muscle activity.

Subjects/Keywords: Kinesiology; Laboratory and Basic Science Research; Other Neuroscience and Neurobiology; Other Physiology; Physiology

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APA (6^th Edition):

Compton, C. (2018). The fatigue-associated changes in estimates of persistent inward current in human motor neurons. (Thesis). Wilfrid Laurier University. Retrieved from https://scholars.wlu.ca/etd/2082

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Compton, Chris. “The fatigue-associated changes in estimates of persistent inward current in human motor neurons.” 2018. Thesis, Wilfrid Laurier University. Accessed March 07, 2021. https://scholars.wlu.ca/etd/2082.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Compton, Chris. “The fatigue-associated changes in estimates of persistent inward current in human motor neurons.” 2018. Web. 07 Mar 2021.

Vancouver:

Compton C. The fatigue-associated changes in estimates of persistent inward current in human motor neurons. [Internet] [Thesis]. Wilfrid Laurier University; 2018. [cited 2021 Mar 07]. Available from: https://scholars.wlu.ca/etd/2082.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Compton C. The fatigue-associated changes in estimates of persistent inward current in human motor neurons. [Thesis]. Wilfrid Laurier University; 2018. Available from: https://scholars.wlu.ca/etd/2082

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Kennesaw State University

10. Serpa, Bradley. Modeling and Mapping Addiction in the Zebrafish, Danio rerio.

Degree: MSIB, Biology, 2018, Kennesaw State University

URL: https://digitalcommons.kennesaw.edu/integrbiol_etd/35

► Driven by the communication of dopamine, the vertebrate reward system has been evolutionarily conserved to maintain survival and optimize fitness. The neural circuits governing… (more)

▼ Driven by the communication of dopamine, the vertebrate reward system has been evolutionarily conserved to maintain survival and optimize fitness. The neural circuits governing this system integrate sensory stimuli to produce appropriate, self-preserving responses that underlie experience-based learning. In the most primitive vertebrates, dopamine release in neuronal circuits drives homeostatic behaviors, such as seeking nutrients, finding a mate, or avoiding danger. From agnathans to mammals, dopaminergic synthesis and signaling genes and molecules, along with neuronal pathways and reward system-based behaviors, remain highly conserved. Dopamine signaling proteins include two classes of metabotropic G-Protein Receptor Coupled Dopamine Receptors, D1-like (DRD1) and D2-like (DRD2). DRD1 stimulate the neuron by upregulating adenylate cyclase activity, while DRD2 inhibits neurons by blocking or down-regulating adenylate cyclase. Though greatly conserved, the reward system can be hijacked by chemicals that trigger the release of dopamine. Drugs of abuse, like amphetamines, for instance, increase dopamine availability to trigger reward circuits, leading to addiction behaviors. The mechanisms by which amphetamines stimulate dopamine release among reward neurons and the addiction behaviors expressed have not yet been modeled and correlated in zebrafish, a viable translational model for studying drug addiction. In the present study, addictive behaviors in zebrafish were elicited after fish were exposed to amphetamines through a condition place preference paradigm. After the conditioning period, amphetamine-treated fish spent significantly more time in an experimental tank compartment that was paired with amphetamine exposure (p = 0.0031). Likewise, THC (p = 0.0393) and the anesthetic, MS222 (p = 0.0290) significantly affected time spent in the non-preferred tank compartment after conditioning. Amphetamine-treated fish also displayed unique and heightened anxiety and vigilance behaviors. These behaviors and the influence of amphetamines on conditioned learning are likely stimulated by the increased expression of DRD1 receptors measured in dopaminergic brain areas in the fish compared to controls. These data support the hypothesis that drugs of abuse like amphetamines trigger the communication of dopamine among reward circuit neurons. Advisors/Committee Members: Susan Smith, Martin Hudson.

Subjects/Keywords: Dopamine; Dopamine receptors; neuroadaptation; Aquaculture and Fisheries; Behavioral Neurobiology; Biology; Developmental Neuroscience; Integrative Biology; Molecular and Cellular Neuroscience; Nervous System; Other Neuroscience and Neurobiology; Systems Neuroscience

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APA (6^th Edition):

Serpa, B. (2018). Modeling and Mapping Addiction in the Zebrafish, Danio rerio. (Thesis). Kennesaw State University. Retrieved from https://digitalcommons.kennesaw.edu/integrbiol_etd/35

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Serpa, Bradley. “Modeling and Mapping Addiction in the Zebrafish, Danio rerio.” 2018. Thesis, Kennesaw State University. Accessed March 07, 2021. https://digitalcommons.kennesaw.edu/integrbiol_etd/35.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Serpa, Bradley. “Modeling and Mapping Addiction in the Zebrafish, Danio rerio.” 2018. Web. 07 Mar 2021.

Vancouver:

Serpa B. Modeling and Mapping Addiction in the Zebrafish, Danio rerio. [Internet] [Thesis]. Kennesaw State University; 2018. [cited 2021 Mar 07]. Available from: https://digitalcommons.kennesaw.edu/integrbiol_etd/35.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Serpa B. Modeling and Mapping Addiction in the Zebrafish, Danio rerio. [Thesis]. Kennesaw State University; 2018. Available from: https://digitalcommons.kennesaw.edu/integrbiol_etd/35

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

11. Richardson, Benjamin P. Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians.

Degree: MS, Experimental Psychology, 2015, Central Washington University

URL: https://digitalcommons.cwu.edu/etd/266

► The current study examines the P300 brainwave and working memory differences between musicians and non-musicians. Differences in aspects of recorded electrical brain activity have been… (more)

Subjects/Keywords: Cognitive Neuroscience; EEG; Music Cognition; ERP; Cognition and Perception; Cognitive Neuroscience; Cognitive Psychology; Laboratory and Basic Science Research; Neuroscience and Neurobiology; Other Neuroscience and Neurobiology; Psychology; Social and Behavioral Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Richardson, B. P. (2015). Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians. (Masters Thesis). Central Washington University. Retrieved from https://digitalcommons.cwu.edu/etd/266

Chicago Manual of Style (16^th Edition):

Richardson, Benjamin P. “Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians.” 2015. Masters Thesis, Central Washington University. Accessed March 07, 2021. https://digitalcommons.cwu.edu/etd/266.

MLA Handbook (7^th Edition):

Richardson, Benjamin P. “Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians.” 2015. Web. 07 Mar 2021.

Vancouver:

Richardson BP. Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians. [Internet] [Masters thesis]. Central Washington University; 2015. [cited 2021 Mar 07]. Available from: https://digitalcommons.cwu.edu/etd/266.

Council of Science Editors:

Richardson BP. Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians. [Masters Thesis]. Central Washington University; 2015. Available from: https://digitalcommons.cwu.edu/etd/266

University of Kentucky

12. Keeney, Jeriel T. DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION.

Degree: 2013, University of Kentucky

URL: https://uknowledge.uky.edu/chemistry_etds/27

► The works presented in this dissertation provide insights into the mechanisms of chemotherapy-induced cognitive impairment (CICI or “ChemoBrain”) and take steps toward outlining a preventive… (more)

▼ The works presented in this dissertation provide insights into the mechanisms of chemotherapy-induced cognitive impairment (CICI or “ChemoBrain”) and take steps toward outlining a preventive strategy. CICI is now widely recognized as a complication of cancer chemotherapy experienced by a large percentage of cancer survivors. Approximately fifty percent of existing FDA-approved anti-cancer drugs generate reactive oxygen species (ROS). Doxorubicin (Dox), a prototypical ROS-generating chemotherapeutic agent, produces the reactive superoxide radical anion (O2-•) in vivo. Dox treatment results in oxidation of plasma proteins, including ApoA-I, leading to TNF-α-mediated oxidative stress in plasma and brain. TNF-α elevation in brain leads to further central nervous system toxicity including mitochondrial dysfunction, neuronal death, and cognitive impairment. Co-administration of the antioxidant drug, 2-mercaptoethane sulfonate sodium (MESNA), prevents Dox-induced protein oxidation and subsequent TNF-α elevation in plasma without interfering with the cancer-killing ability of Dox. In studies presented in this dissertation, we measured oxidative stress in both brain and plasma of Dox-treated mice both with and without MESNA. MESNA ameliorated Dox-induced oxidative protein damage in plasma, confirming our prior studies, and in a new finding led to decreased oxidative stress in brain. Using novel object recognition (NOR), we demonstrated the Dox administration resulted in memory deficits. Using hydrogen magnetic resonance imaging spectroscopy (H1-MRS) techniques, we demonstrated that Dox administration led to a dramatic decrease in choline(phosphocholine)/creatine (Cho/Cr) ratios in mouse hippocampus. The activities of both phosphatidylcholine-specific phospholipase C (PC-PLC) and phospholipase D(PLD) were severely diminished following Dox administration. The activity of PC-PLC was preserved when MESNA was co-administered with Dox. In the absence of TNF-α, MRS-indexed Cho/Cr ratio, PLD activity, and mitochondrial oxygen consumption are preserved in brain, and markers of oxidative stress are reduced. Together with results from our previous studies, these results provide strong evidence that TNF-α is strongly associated, if not responsible for CICI. We also tested the notion that O2-• is responsible for Dox-induced plasma protein oxidation and TNF-α release. O2-• resulted in increased oxidative damage to proteins when added to plasma and increased levels of TNF-α in macrophage culture, providing strong evidence that O2-• is responsible for these Dox-induced toxicities.

Subjects/Keywords: brain; cognitive impairment; chemotherapy; TNF-alpha; MESNA; Biochemistry; Cognitive Neuroscience; Molecular and Cellular Neuroscience; Oncology; Other Neuroscience and Neurobiology

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APA (6^th Edition):

Keeney, J. T. (2013). DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/chemistry_etds/27

Chicago Manual of Style (16^th Edition):

Keeney, Jeriel T. “DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION.” 2013. Doctoral Dissertation, University of Kentucky. Accessed March 07, 2021. https://uknowledge.uky.edu/chemistry_etds/27.

MLA Handbook (7^th Edition):

Keeney, Jeriel T. “DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION.” 2013. Web. 07 Mar 2021.

Vancouver:

Keeney JT. DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION. [Internet] [Doctoral dissertation]. University of Kentucky; 2013. [cited 2021 Mar 07]. Available from: https://uknowledge.uky.edu/chemistry_etds/27.

Council of Science Editors:

Keeney JT. DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION. [Doctoral Dissertation]. University of Kentucky; 2013. Available from: https://uknowledge.uky.edu/chemistry_etds/27

Carnegie Mellon University

13. Wen, Jing. Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex.

Degree: 2012, Carnegie Mellon University

URL: http://repository.cmu.edu/dissertations/121

► Experience-dependent plasticity is the adaptability of brain circuits as a result of changes in neural activity, a phenomenon that has been proposed as the neural… (more)

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Wen, J. (2012). Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex. (Thesis). Carnegie Mellon University. Retrieved from http://repository.cmu.edu/dissertations/121

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wen, Jing. “Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex.” 2012. Thesis, Carnegie Mellon University. Accessed March 07, 2021. http://repository.cmu.edu/dissertations/121.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wen, Jing. “Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex.” 2012. Web. 07 Mar 2021.

Vancouver:

Wen J. Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex. [Internet] [Thesis]. Carnegie Mellon University; 2012. [cited 2021 Mar 07]. Available from: http://repository.cmu.edu/dissertations/121.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wen J. Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex. [Thesis]. Carnegie Mellon University; 2012. Available from: http://repository.cmu.edu/dissertations/121

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Loyola University Chicago

14. Petrunich Rutherford, Maureen Lynn. Serotonin 1A Receptor Signaling in the Hypothalamic Paraventricular Nucleus of the Peripubertal Rat.

Degree: PhD, Neuroscience, 2011, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss_6mos/4

► Serotonin (5-HT) is a ubiquitous neurotransmitter in the brain that is involved in various physiologic functions including the regulation of hypothalamic hormones and has… (more)

▼ Serotonin (5-HT) is a ubiquitous neurotransmitter in the brain that is involved in various physiologic functions including the regulation of hypothalamic hormones and has been implicated in various mood disorders such as depression. Preclinical and clinical data from studies in adults have shown that antidepressant drugs produce time-dependent changes in serotonergic and other systems and can also normalize dysfunction associated with the hypothalamic-pituitary-adrenal (HPA) axis. To date, our understanding of the mechanisms of 5-HT receptor signaling and the actions of drugs on serotonergic function have been derived from extensive preclinical research carried out using cell lines in vitro or in adult animal models in vivo. Fewer studies have investigated serotonergic signaling mechanisms or the effects of antidepressants (i.e., selective serotonin reuptake inhibitors (SSRIs)) in animal models prior to sexual maturation. This is a scientific and clinically relevant issue as (1) SSRIs, the most effective pharmacological option for treating mood disorders in children and adolescents, are being increasingly prescribed and may be associated with suicidal thoughts or behaviors in these age groups and (2) preclinical studies in rodents indicate that SSRI-induced modulation of the serotonergic system prior to sexual maturation produces effects that are distinct and more long-lasting than those produced in adults. To date, few if any studies have investigated mechanisms of 5-HT receptor signal transduction in peripubertal hypothalamic neurons in vivo and their regulation by SSRIs, despite a wealth of existing comparative data on serotonin 1A (5-HT1A) receptor signaling in adult hypothalamic rat paraventricular nucleus (PVN). Given the clinical relevance of potential age-dependent differences in serotonergic signaling and regulation of hypothalamic function, the objective of the studies in this dissertation was to identify and characterize the mechanisms of 5-HT1A receptor signaling in the peripubertal hypothalamic PVN. The data generated by studies in this dissertation project provide the first in vivo evidence that 5-HT1A receptors in the peripubertal PVN can activate multiple responses: (1) oxytocin and adrenocorticotropic hormone (ACTH) plasma hormone responses, (2) activation of extracellular signal-regulated kinase (ERK), and (3) activation of protein kinase B (Akt). The data also demonstrate that these pathways may be differentially responsive to different classes of 5-HT1A receptor agonists. (+)8-OH-DPAT (an aminotetralin), acted as a "full" agonist on each of the respective pathways, while tandospirone (an azapirone) exhibited "partial" agonist activity on activation of Akt but exhibited "full" agonist activity on neuroendocrine responses and activation of ERK. 5-HT1A receptors produce a rapid and prolonged activation of ERK in the peripubertal PVN, unlike the rapid but more transient response in the adult PVN. In addition, the 5-HT1A activation of ERK may be expressed only in certain…

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Petrunich Rutherford, M. L. (2011). Serotonin 1A Receptor Signaling in the Hypothalamic Paraventricular Nucleus of the Peripubertal Rat. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss_6mos/4

Chicago Manual of Style (16^th Edition):

Petrunich Rutherford, Maureen Lynn. “Serotonin 1A Receptor Signaling in the Hypothalamic Paraventricular Nucleus of the Peripubertal Rat.” 2011. Doctoral Dissertation, Loyola University Chicago. Accessed March 07, 2021. https://ecommons.luc.edu/luc_diss_6mos/4.

MLA Handbook (7^th Edition):

Petrunich Rutherford, Maureen Lynn. “Serotonin 1A Receptor Signaling in the Hypothalamic Paraventricular Nucleus of the Peripubertal Rat.” 2011. Web. 07 Mar 2021.

Vancouver:

Petrunich Rutherford ML. Serotonin 1A Receptor Signaling in the Hypothalamic Paraventricular Nucleus of the Peripubertal Rat. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2011. [cited 2021 Mar 07]. Available from: https://ecommons.luc.edu/luc_diss_6mos/4.

Council of Science Editors:

Petrunich Rutherford ML. Serotonin 1A Receptor Signaling in the Hypothalamic Paraventricular Nucleus of the Peripubertal Rat. [Doctoral Dissertation]. Loyola University Chicago; 2011. Available from: https://ecommons.luc.edu/luc_diss_6mos/4

Loyola University Chicago

15. Shaw, Maureen Ashlee. Spartin Protein Associates with Phospholipids Via Its Plant-Related Senescence Domain and Functions as a Lipid Transfer Protein.

Degree: MS, Neuroscience, 2012, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_theses_1yr/1

► Troyer syndrome is a hereditary spastic paraplegia caused by a mutation that leads to a complete loss of expression of spartin protein. The plant-related… (more)

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Shaw, M. A. (2012). Spartin Protein Associates with Phospholipids Via Its Plant-Related Senescence Domain and Functions as a Lipid Transfer Protein. (Thesis). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_theses_1yr/1

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shaw, Maureen Ashlee. “Spartin Protein Associates with Phospholipids Via Its Plant-Related Senescence Domain and Functions as a Lipid Transfer Protein.” 2012. Thesis, Loyola University Chicago. Accessed March 07, 2021. https://ecommons.luc.edu/luc_theses_1yr/1.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shaw, Maureen Ashlee. “Spartin Protein Associates with Phospholipids Via Its Plant-Related Senescence Domain and Functions as a Lipid Transfer Protein.” 2012. Web. 07 Mar 2021.

Vancouver:

Shaw MA. Spartin Protein Associates with Phospholipids Via Its Plant-Related Senescence Domain and Functions as a Lipid Transfer Protein. [Internet] [Thesis]. Loyola University Chicago; 2012. [cited 2021 Mar 07]. Available from: https://ecommons.luc.edu/luc_theses_1yr/1.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shaw MA. Spartin Protein Associates with Phospholipids Via Its Plant-Related Senescence Domain and Functions as a Lipid Transfer Protein. [Thesis]. Loyola University Chicago; 2012. Available from: https://ecommons.luc.edu/luc_theses_1yr/1

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Wisconsin – Milwaukee

16. Tuscher, Jennifer. The Role of Hippocampal and Medial Prefrontal Interactions in the Estrogenic Regulation of Memory.

Degree: PhD, Psychology, 2017, University of Wisconsin – Milwaukee

URL: https://dc.uwm.edu/etd/1716

► Dendritic spine plasticity is thought to be essential for the formation and storage of memories. The sex-steroid hormone 17-estradiol (E2) increases dendritic spine density… (more)

▼ Dendritic spine plasticity is thought to be essential for the formation and storage of memories. The sex-steroid hormone 17-estradiol (E2) increases dendritic spine density in 2 brain regions necessary for memory formation, the dorsal hippocampus (DH) and medial prefrontal cortex (mPFC), but the mechanisms through which it does so remain largely unknown. Further, the extent to which these brain regions interact to mediate E2’s effects on memory is also unclear. Recently, we found that infusion of E2 directly into the DH also increases dendritic spine density in the DH and mPFC, and that these effects depend upon rapid activation of the extracellular signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) cell-signaling pathways in the DH (Tuscher et al., 2016). These intriguing findings highlighted a previously unexplored interaction between the DH and mPFC that may have important implications for understanding how E2 regulates memory. As such, these data led us to question what the role of the mPFC is during object memory formation, and whether interactions between the DH and mPFC are necessary for the E2-induced memory enhancements we have previously observed in our object memory tasks (Fernandez et al., 2008, Boulware et al., 2013, Fortress et al., 2013). Therefore the overall goal of the dissertation was to examine the role of the DH and mPFC in object memory consolidation both in the presence and absence of exogenous E2 infusions, and to examine how E2 regulates spine density changes in these regions, which may ultimately strengthen the synaptic connections involved in the formation of such memories. To this end, we first utilized inhibitory Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to inactivate the DH, the mPFC, or both brain regions simultaneously immediately after novel object training to assess the role of each of these regions individually and in combination during object memory consolidation. Next, we asked whether E2 can act directly in the mPFC to enhance object memory consolidation and increase spine density in the mPFC and DH. Finally, we combined DREADD-mediated inhibition of the mPFC with direct infusion of E2 into the DH to examine whether DH-mPFC interactions are necessary for the beneficial mnemonic effects of DH infused E2. Our results collectively suggest that individual and simultaneous activation of both the DH and mPFC is required for the successful consolidation of object recognition and spatial memories. We also found that infusion of E2 directly into the mPFC increases mPFC apical spine density and facilitates object memory consolidation. Finally, we demonstrate that activation of the mPFC is necessary for the memory-enhancing effects of DH-infused E2. Together, these studies provide critical insight into how the DH and mPFC work in concert to facilitate E2-mediated memory enhancement in female mice. Further, this work will enable future studies investigating circuit and cellular-level questions regarding how E2 mediates cognition across the… Advisors/Committee Members: Karyn Frick.

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tuscher, J. (2017). The Role of Hippocampal and Medial Prefrontal Interactions in the Estrogenic Regulation of Memory. (Doctoral Dissertation). University of Wisconsin – Milwaukee. Retrieved from https://dc.uwm.edu/etd/1716

Chicago Manual of Style (16^th Edition):

Tuscher, Jennifer. “The Role of Hippocampal and Medial Prefrontal Interactions in the Estrogenic Regulation of Memory.” 2017. Doctoral Dissertation, University of Wisconsin – Milwaukee. Accessed March 07, 2021. https://dc.uwm.edu/etd/1716.

MLA Handbook (7^th Edition):

Tuscher, Jennifer. “The Role of Hippocampal and Medial Prefrontal Interactions in the Estrogenic Regulation of Memory.” 2017. Web. 07 Mar 2021.

Vancouver:

Tuscher J. The Role of Hippocampal and Medial Prefrontal Interactions in the Estrogenic Regulation of Memory. [Internet] [Doctoral dissertation]. University of Wisconsin – Milwaukee; 2017. [cited 2021 Mar 07]. Available from: https://dc.uwm.edu/etd/1716.

Council of Science Editors:

Tuscher J. The Role of Hippocampal and Medial Prefrontal Interactions in the Estrogenic Regulation of Memory. [Doctoral Dissertation]. University of Wisconsin – Milwaukee; 2017. Available from: https://dc.uwm.edu/etd/1716

University of Vermont

17. Spohn, Stephanie Nicole. Protective Actions of 5-HT4 Receptors in the Colonic Epithelium.

Degree: PhD, Neuroscience, 2016, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/484

► 5-HT4 receptors are expressed in colonic epithelium, and activation with 5-HT4 receptor agonists causes a number of responses, including mucus secretion from goblet cells,… (more)

▼ 5-HT4 receptors are expressed in colonic epithelium, and activation with 5-HT4 receptor agonists causes a number of responses, including mucus secretion from goblet cells, chloride secretion from enterocytes, and 5-HT release from enterochromaffin cells. We tested whether this receptor could serve a protective role in models of colitis and under basal conditions. Male CD-1 mice (Charles River, Canada) were administered dextran sodium sulfate (DSS; 4% w/v in tap water, MW: 40,000) or trinitrobenzene sulfonic acid (TNBS; 7.5mg/mL in 50% ethanol by enema) on day 0. Treatment with the 5-HT4 receptor agonist, tegaserod (1 mg/Kg), or agonist plus the antagonist, GR113808 (1 mg/Kg), began either 24 hours after colitis induction and continued daily for 6 days (prevention paradigm), or 5 days after colitis was induced and continued for 10 days (recovery paradigm). To test for an action of 5-HT4 receptors under basal conditions, the antagonist, GR113808 was administered to normal mice by daily enema for 10 days. Colitis was evaluated using disease activity index (DAI) and histological damage scores (HDS). Possible protective mechanisms such as improved epithelial barrier function were evaluated by cell proliferation by Ki-67 immunostaining, whereas cell migration and resistance to oxidative stress were explored in CaCo-2 cells. We also tested the effects of tegaserod and/or GR113808 on colonic motility in guinea pigs, a well described model of colonic function. Treatment with tegaserod by enema in both DSS and TNBS-inflamed animals significantly attenuated the development of colitis, and accelerated recovery from established colitis, and these effects were blocked by 5-HT4 antagonist treatment. This effect was not seen when tegaserod was administered by intraperitoneal injection. TNBS-induced dysmotility in guinea pigs was significantly reversed by 5-HT4 receptor agonist treatment, but dysmotility persisted in animals treated with the agonist plus antagonist. We observed significant increases in the proportion of epithelial cells that were Ki-67 positive in DSS-inflamed mice treated with the agonist, and this effect was blocked by the antagonist. In CaCo-2 cells, 5-HT4 receptor activation accelerated cell migration into scratches on cell cultures, and increased resistance to oxidative stress-induced apoptosis, and these effects were blocked by the antagonist. Furthermore, treatment with the antagonist alone resulted in significant increases in disease activity index, histological damage scores and bacterial translocation in mice, and led to disrupted motility patterns in guinea pig distal colon. 5-HT4 receptor stimulation reduced the development of, and accelerated the recovery from, inflammation. These effects likely involved improved wound healing and resistance to oxidative stress. Interestingly, inhibition of 5-HT4 activity in normal animals resulted in inflammation, decreased epithelial proliferation and disrupted motility. Taken together, these data suggest that… Advisors/Committee Members: Gary M. Mawe.

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Spohn, S. N. (2016). Protective Actions of 5-HT4 Receptors in the Colonic Epithelium. (Doctoral Dissertation). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/484

Chicago Manual of Style (16^th Edition):

Spohn, Stephanie Nicole. “Protective Actions of 5-HT4 Receptors in the Colonic Epithelium.” 2016. Doctoral Dissertation, University of Vermont. Accessed March 07, 2021. https://scholarworks.uvm.edu/graddis/484.

MLA Handbook (7^th Edition):

Spohn, Stephanie Nicole. “Protective Actions of 5-HT4 Receptors in the Colonic Epithelium.” 2016. Web. 07 Mar 2021.

Vancouver:

Spohn SN. Protective Actions of 5-HT4 Receptors in the Colonic Epithelium. [Internet] [Doctoral dissertation]. University of Vermont; 2016. [cited 2021 Mar 07]. Available from: https://scholarworks.uvm.edu/graddis/484.

Council of Science Editors:

Spohn SN. Protective Actions of 5-HT4 Receptors in the Colonic Epithelium. [Doctoral Dissertation]. University of Vermont; 2016. Available from: https://scholarworks.uvm.edu/graddis/484

University of Vermont

18. Pappas, Anthony Christ. Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling.

Degree: PhD, Neuroscience, 2016, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/475

► Deficits within the brain microcirculation contribute to poor patient outcome following aneurysmal subarachnoid hemorrhage (SAH). However, the underlying pathophysiology is not well understood. Intra-cerebral… (more)

▼ Deficits within the brain microcirculation contribute to poor patient outcome following aneurysmal subarachnoid hemorrhage (SAH). However, the underlying pathophysiology is not well understood. Intra-cerebral (parenchymal) arterioles are encased by specialized glial processes, called astrocyte endfeet. Ca2+ signals in the endfeet, driven by the ongoing pattern of neuronal activity, regulate parenchymal arteriolar diameter and thereby influence local cerebral blood flow. In the healthy brain, this phenomenon, called neurovascular coupling (NVC), matches focal increases in neuronal activity with local arteriolar dilation. This ensures adequate delivery of oxygen and other nutrients to areas of the brain with increased metabolic demand. Recently, we demonstrated inversion of NVC from vasodilation to vasoconstriction in brain slices obtained from SAH model animals. This pathological change, which would restrict blood flow to active brain regions, was accompanied by an increase in the amplitude of spontaneous Ca2+ events in astrocyte endfeet. It is possible that the emergence of higher amplitude endfoot Ca2+ events shifts the polarity of NVC after SAH by elevating levels of vasoactive agents (e.g. K+ ions) within the perivascular space. In the first aim of this dissertation we tested whether altered endfoot Ca2+ signaling underlies the inversion of NVC after SAH. Brain injury is often associated with increased levels of extracellular purine nucleotides (e.g. ATP). A recent study found that ATP levels in the cerebrospinal fluid of aneurysmal SAH patients were roughly 400-fold higher than that of non-SAH controls. Astrocytes express a variety of purinergic (P2) receptors that, when activated, could trigger a spike in intra-cellular Ca2+. It is possible that enhanced signaling via astrocyte P2 receptors underlies the change in endfoot Ca2+ signaling after SAH. In the second aim of this dissertation we determined the role of purinergic signaling in the generation of high-amplitude spontaneous endfoot Ca2+ events after SAH. Parenchymal arteriolar diameter and endfoot Ca2+ dynamics were recorded simultaneously in fluo-4-loaded rat brain slices using combined infrared-differential interference contrast and multi-photon fluorescence microscopy. We report that SAH led to a time-dependent emergence of spontaneous endfoot high-amplitude Ca2+ signals (eHACSs) that were only present in brain slices exhibiting inversion of NVC. Depletion of intracellular Ca2+ stores abolished spontaneous endfoot Ca2+ signals, including eHACSs, and restored arteriolar dilation in SAH brain slices to two downstream elements in the NVC signaling cascade, (1) increased endfoot Ca2+ and (2) elevated extracellular K+. We next tested the role of purinergic signaling in the generation of SAH-induced eHACSs by recording endfoot activity before and after treatment with the broad-spectrum purinergic receptor antagonist, suramin. Remarkably, suramin selectively abolished eHACSs and restored vasodilatory NVC in SAH brain slices. Desensitization of… Advisors/Committee Members: George C. Wellman, Jeffrey L. Spees.

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Pappas, A. C. (2016). Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling. (Doctoral Dissertation). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/475

Chicago Manual of Style (16^th Edition):

Pappas, Anthony Christ. “Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling.” 2016. Doctoral Dissertation, University of Vermont. Accessed March 07, 2021. https://scholarworks.uvm.edu/graddis/475.

MLA Handbook (7^th Edition):

Pappas, Anthony Christ. “Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling.” 2016. Web. 07 Mar 2021.

Vancouver:

Pappas AC. Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling. [Internet] [Doctoral dissertation]. University of Vermont; 2016. [cited 2021 Mar 07]. Available from: https://scholarworks.uvm.edu/graddis/475.

Council of Science Editors:

Pappas AC. Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling. [Doctoral Dissertation]. University of Vermont; 2016. Available from: https://scholarworks.uvm.edu/graddis/475

University of Vermont

19. D'Alberto, Nicholas C. Examining Inter- And Intra-Individual Differences In The Neurobiological Mechanisms Associated With Inhibitory Control.

Degree: PhD, Neuroscience, 2018, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/962

► Adolescence is an ideal time to measure the development of the neural mechanisms associated with inhibitory control because this age period is marked by… (more)

▼ Adolescence is an ideal time to measure the development of the neural mechanisms associated with inhibitory control because this age period is marked by impulsive and risk taking behaviors. Maturational brain changes in the prefrontal cortex that are associated with the emergence of inhibitory control are thought to occur during this age. With knowledge of how this system develops, it may be possible to identify the development of disorders that arise from poor inhibitory control such as attention deficit hyperactivity disorder (ADHD) and substance use. The goal of the current dissertation is to examine the neurobiological correlates associated with individual differences in inhibitory ability, and examine the age-related changes in neurobiological mechanisms of inhibitory control. This report will be the first of its size (n = 538) to examine within-subject changes longitudinally over five years of adolescent development (age 14 to 19). Furthermore, we supplement the longitudinal data with findings from a split-brain patient on the lateralization of inhibitory control, and we explore a subtle nuance that may have large implications on how to best measure inhibition-related brain activity. In the second chapter of the dissertation, we examine the lateralization of inhibitory control by measuring hemispheric differences in the ability to inhibit a motor response in a split-brain patient. Here, we found patient J.W.’s right hemisphere performed better than his left hemisphere on three different inhibitory control tasks. Interestingly, although inferior to the performance of the right hemisphere, the left hemisphere still performed relatively well on the three tasks, suggesting the left hemisphere can perform response inhibition independently. The third chapter examines both the functional correlates of Stop Signal Task performance, and the age-related differences in the functional mechanisms of response inhibition. At age 14 and age 19, similar patterns of activation were associated with performance, however relatively little overall activity exhibited performance-related effects. Superior performance was associated with greater right inferior frontal gyrus (rIFG) activation, as well as greater activation in a set of regions potentially involved with a stimulus-detection and attention-orienting system. However, at age 14 performance was also negatively associated with default mode network activity, and at age 19 performance was also positively associated with left amygdala activity. In the absence of within-subject differences in performance between ages 14 to 19, there were significant decreases in functional activation associated with successful inhibition. The potential mechanisms by which activity decreases over time while performance remains stable are discussed. The fourth chapter of the dissertation examines the effect of objective task difficulty on the magnitude of activation associated with successful inhibition. The Stop Signal Task employs an adaptive… Advisors/Committee Members: Hugh P. Garavan.

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

D'Alberto, N. C. (2018). Examining Inter- And Intra-Individual Differences In The Neurobiological Mechanisms Associated With Inhibitory Control. (Doctoral Dissertation). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/962

Chicago Manual of Style (16^th Edition):

D'Alberto, Nicholas C. “Examining Inter- And Intra-Individual Differences In The Neurobiological Mechanisms Associated With Inhibitory Control.” 2018. Doctoral Dissertation, University of Vermont. Accessed March 07, 2021. https://scholarworks.uvm.edu/graddis/962.

MLA Handbook (7^th Edition):

D'Alberto, Nicholas C. “Examining Inter- And Intra-Individual Differences In The Neurobiological Mechanisms Associated With Inhibitory Control.” 2018. Web. 07 Mar 2021.

Vancouver:

D'Alberto NC. Examining Inter- And Intra-Individual Differences In The Neurobiological Mechanisms Associated With Inhibitory Control. [Internet] [Doctoral dissertation]. University of Vermont; 2018. [cited 2021 Mar 07]. Available from: https://scholarworks.uvm.edu/graddis/962.

Council of Science Editors:

D'Alberto NC. Examining Inter- And Intra-Individual Differences In The Neurobiological Mechanisms Associated With Inhibitory Control. [Doctoral Dissertation]. University of Vermont; 2018. Available from: https://scholarworks.uvm.edu/graddis/962

University of Iowa

20. Stump, Madeliene. The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis.

Degree: PhD, Neuroscience, 2017, University of Iowa

URL: https://ir.uiowa.edu/etd/6000

► The Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a master regulator of adipogenesis, has been shown to influence energy balance through its actions in the brain… (more)

▼ The Peroxisome Proliferator-Activated Receptor gamma (PPARγ), a master regulator of adipogenesis, has been shown to influence energy balance through its actions in the brain rather than in the adipose tissue alone. Deletion of PPARγ in mouse brain results in resistance to weight gain in response to high fat diet. Activation of PPARγ leads to change in the firing pattern of melanocortin system neurons (POMC and AgRP), which are critical for energy homeostasis. To determine the effects of modulation of brain PPARγ on food intake and energy expenditure we generated a novel transgenic mouse model in which a dominant-negative (DN) mutant form of PPARγ (P467L) or a wild type (WT) form that is conditionally expressed in either the entire central nervous system (CNS) or specifically in POMC or AgRP neurons. Interference with brain PPARγ results in impaired insulin and glucose regulation. This in turn has significant implications in altering the growth rate and metabolic homeostasis. In light of the well-established role of PPARγ in regulating insulin sensitivity, this is the first report implicating brain PPARγ in controlling peripheral insulin levels. Overexpression of the WT PPARγ in the CNS leads to failure to thrive and early death due to microcephaly and severe distortion of brain architecture with notable agenesis of the corpus callosum. Our results show that the levels of PPARγ in the brain are tightly regulated and perturbations leading to “too much” or “too little” functional PPARγ result in major shifts in structural organization of the brain or metabolic balance. The herein presented data show that chronic interference with the function of neuronal PPARγ affects energy balance only under certain dietary conditions and through specific neuronal populations. We show that POMC, but not AgRP neurons, are particularly sensitive to modulation of PPARγ activity. These observations give support to the notion that cellular adaptations in POMC neurons, driven by PPARγ, represent critical components in the regulation of metabolic homeostasis. Advisors/Committee Members: Sigmund, Curt Daniel (supervisor).

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Stump, M. (2017). The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/6000

Chicago Manual of Style (16^th Edition):

Stump, Madeliene. “The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis.” 2017. Doctoral Dissertation, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/6000.

MLA Handbook (7^th Edition):

Stump, Madeliene. “The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis.” 2017. Web. 07 Mar 2021.

Vancouver:

Stump M. The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis. [Internet] [Doctoral dissertation]. University of Iowa; 2017. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/6000.

Council of Science Editors:

Stump M. The role of brain PPAR[gamma] in regulation of energy balance and glucose homeostasis. [Doctoral Dissertation]. University of Iowa; 2017. Available from: https://ir.uiowa.edu/etd/6000

University of Iowa

21. Wernett, Pamela Joy. The effects of Med12 variation upon cell cycle progression and differential gene expression.

Degree: PhD, Neuroscience, 2011, University of Iowa

URL: https://ir.uiowa.edu/etd/2787

► MED12 is an X– chromosome member of the Mediator complex that is a key regulator of tissue specific gene expression and moderates intracellular signaling… (more)

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Wernett, P. J. (2011). The effects of Med12 variation upon cell cycle progression and differential gene expression. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/2787

Chicago Manual of Style (16^th Edition):

Wernett, Pamela Joy. “The effects of Med12 variation upon cell cycle progression and differential gene expression.” 2011. Doctoral Dissertation, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/2787.

MLA Handbook (7^th Edition):

Wernett, Pamela Joy. “The effects of Med12 variation upon cell cycle progression and differential gene expression.” 2011. Web. 07 Mar 2021.

Vancouver:

Wernett PJ. The effects of Med12 variation upon cell cycle progression and differential gene expression. [Internet] [Doctoral dissertation]. University of Iowa; 2011. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/2787.

Council of Science Editors:

Wernett PJ. The effects of Med12 variation upon cell cycle progression and differential gene expression. [Doctoral Dissertation]. University of Iowa; 2011. Available from: https://ir.uiowa.edu/etd/2787

University of Iowa

22. Keeler, Austin Byler. Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization.

Degree: PhD, Neuroscience, 2015, University of Iowa

URL: https://ir.uiowa.edu/etd/2230

► Growth of a properly complex dendrite arbor is a vital step in neuronal differentiation and a prerequisite for normal neural circuit formation; likewise, overly… (more)

▼ Growth of a properly complex dendrite arbor is a vital step in neuronal differentiation and a prerequisite for normal neural circuit formation; likewise, overly dense or sparse dendrite arbors are a key feature of abnormal neural circuit formation and characteristic of many neurodevelopmental disorders. Thus, identifying factors involved in aberrant dendrite complexity and therefore aberrant circuit formation, are necessary to understanding these disorders. In my doctoral work I have elucidated both intracellular and extracellular aspects to the gamma-protocadherins (γ-Pcdhs) that regulate dendrite complexity. Loss of the 22 γ-Pcdhs, adhesion molecules that interact homophilically and are expressed combinatorially in neurons and astrocytes, leads to aberrantly high activity of focal adhesion kinase (FAK) and reduced dendrite complexity in cortical neurons. Little is known, however, about how γ-Pcdh function is regulated by other factors. Here I show that PKC phosphorylates a serine residue situated within the shared γ-Pcdh C-terminus; PKC phosphorylation disrupts the γ-Pcdhs’ inhibition of FAK. Additionally, γ-Pcdh phosphorylation or a phosphomimetic mutant reduce dendritic arbors, while blocking γ-Pcdh phosphorylation increases dendrite complexity. Together, these data identify a novel intracellular mechanism through which γ-Pcdh control of a signaling pathway important for dendrite arborization is regulated. Although specific interactions between diverse cell surface molecules are proposed to regulate circuit formation, the extent to which these promote dendrite growth and branching is unclear. Here, using transgenic mice to manipulate expression in vivo, I and my colleagues show that the complexity of a cortical neuron’s dendritic arbor is regulated by γ-Pcdh isoform matching with surrounding cells. Expression of the same single γ-Pcdh isoform leads to exuberant or minimal arbor complexity depending on matched expression of surrounding cells. Additionally, loss of γ-Pcdhs in astrocytes, or induced mis-matching between astrocytes and neurons, reduces dendrite complexity in a cell non-autonomous manner. Thus, these data support our proposal that γ-Pcdhs create a rare neuronal identity that, depending on the identities of surrounding cells, specifies the complexity of that neuron’s dendritic arbor. Advisors/Committee Members: Weiner, Joshua A. (supervisor).

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Keeler, A. B. (2015). Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/2230

Chicago Manual of Style (16^th Edition):

Keeler, Austin Byler. “Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization.” 2015. Doctoral Dissertation, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/2230.

MLA Handbook (7^th Edition):

Keeler, Austin Byler. “Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization.” 2015. Web. 07 Mar 2021.

Vancouver:

Keeler AB. Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/2230.

Council of Science Editors:

Keeler AB. Branching out by sticking together: elucidating mechanisms of gamma-protocadherin control of dendrite arborization. [Doctoral Dissertation]. University of Iowa; 2015. Available from: https://ir.uiowa.edu/etd/2230

University of Iowa

23. Thomas, Jessica René. Elucidating the molecular and biophysical determinants that suppress Ca2+-dependent facilitation of Cav2.2 Ca2+ channels.

Degree: PhD, Neuroscience, 2018, University of Iowa

URL: https://ir.uiowa.edu/etd/6307

► Cav2.2 channels are presynaptic voltage-gated Ca2+ channels that regulate neurotransmitter release. In addition, they are major therapeutic targets from neuropathic pain, a chronic pain… (more)

▼ Cav2.2 channels are presynaptic voltage-gated Ca2+ channels that regulate neurotransmitter release. In addition, they are major therapeutic targets from neuropathic pain, a chronic pain disorder caused by injury to the nerve. Pain-relieving drugs such as opioids and ziconotide block Cav2.2 channels. Unfortunately, these drugs are associated with severe adverse side effects. Therefore, there is a need to understand the factors that regulate Cav2.2 channels to design more effective therapies. My dissertation uses electrophysiological techniques to understand the factors that regulate Cav2.2 channel function. My research will provide insights into how Cav2.2 channels integrate diverse cellular signals to shape neurotransmission. This knowledge can be used to treat neurological disorders, such as chronic pain and Myoclonus- Dystonia syndrome, a movement disorder associated with a mutation in the gene that encodes Cav2.2. A variety of regulatory mechanisms modulate Ca2+ entry through Cav2.2 channels. One prominent from of regulation is Ca2+-dependent inactivation, a negative feedback mechanism. Incoming Ca2+ ions bind to the Ca2+ sensor calmodulin, which is tethered to the channel. The interaction between Ca2+ and calmodulin is thought to induce a conformational change in the structure of Cav2.2 to reduce further Ca2+ entry. The related voltage-gated Ca2+ channel Cav2.1 undergoes an additional and opposing form of regulation, Ca2+-dependent facilitation, which enhances Ca2+ entry. Ca2+-dependent inactivation and facilitation of Cav2.1 can adjust the amount of neurotransmitter released at a synapse in ways that modify information processing in the nervous system. Unlike Cav2.1, Cav2.2 does not undergo Ca2+-dependent facilitation, but the mechanism underlying this difference is unknown. One possibility is that Cav2.2 channels do not contain the molecular components necessary to support Ca2+-dependent facilitation, which have been identified in Cav2.1 in previous studies. I hypothesized that the analogous regions of Cav2.2 contain slight modifications, which prevents Ca2+-dependent facilitation. In support of this hypothesis, I found that Cav2.2 channels can undergo Ca2+-dependent facilitation upon transferring portions of the C-terminal domain of Cav2.1 to Cav2.2. A second possibility is that Cav2.2 undergoes other forms of regulation that oppose Ca2+-dependent facilitation. Cav2.2 is strongly inhibited by ligands for some G protein-coupled receptors, which helps prevent excess release of neurotransmitters in the nervous system. I hypothesized that strong G protein modulation of Cav2.2 opposes Ca2+-dependent facilitation. I found that Cav2.2 channels could undergo a form of Ca2+-dependent facilitation upon inhibiting G-protein signaling, which supported my hypothesis. Taken together, my results demonstrate that multiple factors contribute the lack of Ca2+-dependent facilitation observed for Cav2.2 channels. My results provide new insights into the intrinsic and extrinsic forces that regulate… Advisors/Committee Members: Lee, Amy (supervisor).

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Thomas, J. R. (2018). Elucidating the molecular and biophysical determinants that suppress Ca2+-dependent facilitation of Cav2.2 Ca2+ channels. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/6307

Chicago Manual of Style (16^th Edition):

Thomas, Jessica René. “Elucidating the molecular and biophysical determinants that suppress Ca2+-dependent facilitation of Cav2.2 Ca2+ channels.” 2018. Doctoral Dissertation, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/6307.

MLA Handbook (7^th Edition):

Thomas, Jessica René. “Elucidating the molecular and biophysical determinants that suppress Ca2+-dependent facilitation of Cav2.2 Ca2+ channels.” 2018. Web. 07 Mar 2021.

Vancouver:

Thomas JR. Elucidating the molecular and biophysical determinants that suppress Ca2+-dependent facilitation of Cav2.2 Ca2+ channels. [Internet] [Doctoral dissertation]. University of Iowa; 2018. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/6307.

Council of Science Editors:

Thomas JR. Elucidating the molecular and biophysical determinants that suppress Ca2+-dependent facilitation of Cav2.2 Ca2+ channels. [Doctoral Dissertation]. University of Iowa; 2018. Available from: https://ir.uiowa.edu/etd/6307

University of Iowa

24. Alberico, Stephanie Lorraine. Striatal neurons in the development of levodopa-induced dyskinesias in Parkinson’s disease.

Degree: PhD, Neuroscience, 2017, University of Iowa

URL: https://ir.uiowa.edu/etd/5903

► Levodopa-induced dyskinesias (LIDs) are abnormal involuntary movements that limit the effectiveness of treatments for Parkinson’s disease. Although dyskinesias involve the striatum, it is unclear… (more)

▼ Levodopa-induced dyskinesias (LIDs) are abnormal involuntary movements that limit the effectiveness of treatments for Parkinson’s disease. Although dyskinesias involve the striatum, it is unclear how striatal neurons are involved in dyskinetic movements. Here we record from striatal neurons in mice during levodopa-induced axial dyskinesias. We developed an automated 3-dimensional motion tracking system to capture the development of axial dyskinesias at ~10 ms resolution, and correlated these movements with neuronal activity of striatal medium spiny neurons and fast spiking interneurons. The average firing rate of medium spiny neurons increased as axial dyskinesias developed, and both medium spiny neurons and fast spiking interneurons were modulated around axial dyskinesias. We also found that delta field potential power increased in the striatum with dyskinesia, and that this increased delta power coupled with striatal neurons. Secondly, we studied the role of the two main types of dopamine receptors. We pharmacologically inhibited either the D1 or D2 receptors while recording from neuronal ensembles in the striatum and measuring LIDs in high temporal resolution. We found that inhibiting the D1, but not the D2, receptor led to a decrease in axial dyskinesias. Interestingly, both types of antagonist attenuated the strong modulation of MSNs around axial dyskinesias when compared to levodopa alone. These results suggest that LIDs are modulated through activity in D1-MSNs. Lastly, we selectively targeted the D1 receptor expressing neurons (D1-MSNs) with optogenetics. With this technique, we can specifically activate or inhibit certain neuronal populations. We found that stimulating the D1-MSNs led to dyskinetic events only after levodopa priming. However, inhibiting these neurons was not sufficient to attenuate dyskinesias following levodopa administration. We also found that putative D1-MSNs are more strongly modulated around axial dyskinesias than other MSNs. Together, our findings provide novel insight into how striatal networks change as LIDs develop, and suggest that increased medium spiny neuron firing, that D1-MSNs are strongly modulated around LIDs, and that D1-MSN activity is sufficient to drive dyskinesias. These data could help clarify the role of the striatum in the pathogenesis of dyskinesias in Parkinson’s disease. Advisors/Committee Members: Narayanan, Nandakumar (supervisor).

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Alberico, S. L. (2017). Striatal neurons in the development of levodopa-induced dyskinesias in Parkinson’s disease. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/5903

Chicago Manual of Style (16^th Edition):

Alberico, Stephanie Lorraine. “Striatal neurons in the development of levodopa-induced dyskinesias in Parkinson’s disease.” 2017. Doctoral Dissertation, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/5903.

MLA Handbook (7^th Edition):

Alberico, Stephanie Lorraine. “Striatal neurons in the development of levodopa-induced dyskinesias in Parkinson’s disease.” 2017. Web. 07 Mar 2021.

Vancouver:

Alberico SL. Striatal neurons in the development of levodopa-induced dyskinesias in Parkinson’s disease. [Internet] [Doctoral dissertation]. University of Iowa; 2017. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/5903.

Council of Science Editors:

Alberico SL. Striatal neurons in the development of levodopa-induced dyskinesias in Parkinson’s disease. [Doctoral Dissertation]. University of Iowa; 2017. Available from: https://ir.uiowa.edu/etd/5903

University of Pennsylvania

25. Boccitto, Marco. Genetic and Pharmacological Approaches to Preventing Neurodegeneration.

Degree: 2012, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/494

► The Insulin/Insulin-like Growth Factor 1 Signaling (IIS) pathway was first identified as a major modifier of aging in C.elegans. It has since become clear that… (more)

▼ The Insulin/Insulin-like Growth Factor 1 Signaling (IIS) pathway was first identified as a major modifier of aging in C.elegans. It has since become clear that the ability of this pathway to modify aging is phylogenetically conserved. Aging is a major risk factor for a variety of neurodegenerative diseases including the motor neuron disease, Amyotrophic Lateral Sclerosis (ALS). This raises the possibility that the IIS pathway might have therapeutic potential to modify the disease progression of ALS. In a C. elegans model of ALS we found that decreased IIS had a beneficial effect on ALS pathology in this model. This beneficial effect was dependent on activation of the transcription factor daf-16. To further validate IIS as a potential therapeutic target for treatment of ALS, manipulations of IIS in mammalian cells were investigated for neuroprotective activity. Genetic manipulations that increase the activity of the mammalian ortholog of daf-16, FOXO3, were found to be neuroprotective in a series of in vitro models of ALS toxicity. The small molecule Psammaplysene A (PA) is known to increase the nuclear abundance of FOXO3. PA was also found to be protective in mammalian in vitro models of ALS toxicity as well as a fly and worm model of neurodegeneration. Due to the wide variety of neurodegenerative diseases that share aging as a risk factor, a small molecule modifier of FOXO/daf-16 such as PA could hold great therapeutic potential. Most clinically viable drugs have certain physico-chemical properties that fall within a well-defined set of values, which unfortunately PA does not share. Due to its poor "drug-likness", an investigation into the mechanism of action of PA was undertaken in order to potentially identify more "drug-like" compounds with similar activities. This investigation revealed the heterogeneous nuclear ribonucleoprotein K (HNRNPK) is a direct physical target of PA. PA modifies the ability of HNRNPK to stabilize rRNA but does not affect many of HNRNPK's other functions. How changes in rRNA stability modify IIS or whether these changes definitively underlie PA's neuroprotective mechanism remains to be determined.

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Boccitto, M. (2012). Genetic and Pharmacological Approaches to Preventing Neurodegeneration. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/494

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Boccitto, Marco. “Genetic and Pharmacological Approaches to Preventing Neurodegeneration.” 2012. Thesis, University of Pennsylvania. Accessed March 07, 2021. https://repository.upenn.edu/edissertations/494.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Boccitto, Marco. “Genetic and Pharmacological Approaches to Preventing Neurodegeneration.” 2012. Web. 07 Mar 2021.

Vancouver:

Boccitto M. Genetic and Pharmacological Approaches to Preventing Neurodegeneration. [Internet] [Thesis]. University of Pennsylvania; 2012. [cited 2021 Mar 07]. Available from: https://repository.upenn.edu/edissertations/494.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Boccitto M. Genetic and Pharmacological Approaches to Preventing Neurodegeneration. [Thesis]. University of Pennsylvania; 2012. Available from: https://repository.upenn.edu/edissertations/494

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Drexel University

26. Yang, Qi. Muscle synergy similarities and differences in the intact, neonatal and adult complete spinal cord injured rats, after injury and following several rehabilitation strategies.

Degree: 2016, Drexel University

URL: http://hdl.handle.net/1860/idea:7157

► Loss of lower limb motor functions is among the most commonly seen effects of spinal cord injuries (SCI). Even with the current modern medical care,… (more)

▼ Loss of lower limb motor functions is among the most commonly seen effects of spinal cord injuries (SCI). Even with the current modern medical care, SCI patients require intense care at high expense. Animal models used for research on SCI may help develop better and lower cost therapies. It is well known that neonatal rats with complete SCI are capable of generating autonomous lumbar stepping, some even achieve independent weight support when tested as adults. On the contrary, rats injured at adult ages have limited recovery after a complete spinal cord injury. What can account for the difference? We hypothesized that neonatal and adult SCI animals’ muscle synergy patterns were distinguished from each other and from the intacts’. Although sharing a lot of similarity, compared to the adult SCI animals, neonatal SCI animals had less synergies merging. Some xiv individual synergies of the neonatal SCIs' might resemble the intact animals more than adult SCIs'. To test the hypothesis, we examined the muscle synergy pattern using locomotor electromyography (EMG) in adult animals injured as neonates (T9/10 complete SCI, n=9), intact adult rats (n=12) and the same adult rats 10~14 days after T9/10 complete SCI (n=9). We found that adult SCI animals’ synergies tended to merge post injury compared to the intact animals. The intacts also deviated from the neonatal and adult SCI animals regarding the correlation of all the synergies and individual synergy to a common synergy template. While sharing some similarity, in some individual synergies’ correlation values to the common template, the neonatal animals were more similar to the adult SCIs shortly after injury than to the intacts. The neonatal synergies appeared to be preserved into adulthood and revealed after adult SCI. If given systematical training, would the synergies of adult SCI animals change with function? And if they do, would the change be the same regardless of the rehabilitation paradigms and recovery outcome? In order to answer these questions, we studied the synergy changes following robot-driven epidural stimulation combined with treadmill training (ES) and robotic assisted treadmill only (TM) systematic long-term training and we compared these to the animals resting in the cage after complete adult SCI. We hypothesized that synergies would tend to merge right after injury. As time went by after injury, the synergies’ spatial structure would be simplified. However, with successful rehabilitation, the further merging and simplification of the synergies were avoided. To investigate the only (TM) systematic long-term training and we compared these to the animals resting in the cage after complete adult SCI. We hypothesized that synergies would tend to merge right after injury. As time went by after injury, the synergies’ spatial structure would be simplified. However, with successful rehabilitation, the further merging and simplification of the synergies were avoided. To investigate the synergies’ relationship to therapeutic methods and efficacy, we trained three… Advisors/Committee Members: Giszter, Simon Francis, 1957-, College of Medicine.

Subjects/Keywords: Neurosciences; Neurobiology; Neuroscience

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APA (6^th Edition):

Yang, Q. (2016). Muscle synergy similarities and differences in the intact, neonatal and adult complete spinal cord injured rats, after injury and following several rehabilitation strategies. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7157

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yang, Qi. “Muscle synergy similarities and differences in the intact, neonatal and adult complete spinal cord injured rats, after injury and following several rehabilitation strategies.” 2016. Thesis, Drexel University. Accessed March 07, 2021. http://hdl.handle.net/1860/idea:7157.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yang, Qi. “Muscle synergy similarities and differences in the intact, neonatal and adult complete spinal cord injured rats, after injury and following several rehabilitation strategies.” 2016. Web. 07 Mar 2021.

Vancouver:

Yang Q. Muscle synergy similarities and differences in the intact, neonatal and adult complete spinal cord injured rats, after injury and following several rehabilitation strategies. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1860/idea:7157.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yang Q. Muscle synergy similarities and differences in the intact, neonatal and adult complete spinal cord injured rats, after injury and following several rehabilitation strategies. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7157

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Washington University in St. Louis

27. Mazuski, Cristina. The Role of VIP SCN Neurons in Circadian Physiology and Behavior.

Degree: PhD, Biology & Biomedical Sciences (Neurosciences), 2017, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/1233

► Located in the ventral hypothalamus, the suprachiasmatic nucleus (SCN) is necessary for entraining daily rhythms in physiology and behavior to environmental cues. Though the… (more)

▼ Located in the ventral hypothalamus, the suprachiasmatic nucleus (SCN) is necessary for entraining daily rhythms in physiology and behavior to environmental cues. Though the 20,000 neurons of the SCN uniformly express GABA, they differ greatly in neuropeptide content. One anatomically and functionally distinct class of neuropeptidergic SCN neurons is vasoactive intestinal polypeptide (VIP). Expressed by approximately 10% of SCN neurons, VIP is necessary for synchronizing single-cell SCN rhythms to produce coherent output and sufficient for entrainment. However, little is known about the firing activity of these neurons releases VIP and results in circadian entrainment. We utilized multielectrode array technology and optogenetics to optically tag VIP neurons expressing Channelrhodopsin-2 (ChR2) following three days of spontaneous activity recordings. We find that VIP neurons have circadian firing rates with two distinct patterns, irregular and tonic, that constitute two separate electrophysiological classes. Using optogenetic stimulation in vitro and in vivo, we show that high frequency firing intervals are sufficient to phase shift and entrain circadian rhythms in gene expression and locomotor activity through VIP release. Interestingly, low frequency firing intervals do not phase shift the SCN in vitro and entrain behavioral rhythms more gradually. We also find that stimulation of VIP neurons can only phase delay and entrain rhythms during late subjective day and early subjective night. We conclude that VIP neurons entrain behavior in a time-of-day- and frequency- dependent manner. Complementary to testing the sufficiency of VIP neuronal firing for entrainment, we tested the necessity of VIP neurons for circadian rhythms in the adult SCN circuit. Using Cre-lox technology in vivo, we triggered adult-onset apoptosis in VIP SCN neurons. We found that over 80% of these mice retained circadian rhythms. We contrast this to Vip null mice, where over 60% lose rhythms. A majority of our mice lacking VIP neurons had decreased locomotor activity periods and increased daily onset variability, which strongly correlated with the intensity of VIP staining. In vitro, deletion of VIP neurons leads to a dramatically reduced amplitude of circadian gene expression and decreases in synchrony on the single-cell level. We conclude that the difference between adult deletion of VIP neurons and Vip null mice suggests a role for VIP in SCN development and in the developed adult circuit VIP neurons are not necessary for rhythmicity. Finally, we dissected the role of VIP SCN neurons in the daily rhythms in glucocorticoids, by characterizing the anatomy of VIP projections and testing the necessity of VIP neurons. We labeled VIP SCN neurons that project dorsally to the paraventricular nucleus of the hypothalamus (PVN) using a two-color tract tracing experiment. We concluded that a small bilateral subset of VIP SCN neurons projects to each side of the PVN. To test VIP neurons function, we deleted VIP SCN neurons in the adult and… Advisors/Committee Members: Erik D. Herzog, Michael Bruchas, Paul Taghert, Tim Holy, John Cirrito.

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mazuski, C. (2017). The Role of VIP SCN Neurons in Circadian Physiology and Behavior. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/1233

Chicago Manual of Style (16^th Edition):

Mazuski, Cristina. “The Role of VIP SCN Neurons in Circadian Physiology and Behavior.” 2017. Doctoral Dissertation, Washington University in St. Louis. Accessed March 07, 2021. https://openscholarship.wustl.edu/art_sci_etds/1233.

MLA Handbook (7^th Edition):

Mazuski, Cristina. “The Role of VIP SCN Neurons in Circadian Physiology and Behavior.” 2017. Web. 07 Mar 2021.

Vancouver:

Mazuski C. The Role of VIP SCN Neurons in Circadian Physiology and Behavior. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2017. [cited 2021 Mar 07]. Available from: https://openscholarship.wustl.edu/art_sci_etds/1233.

Council of Science Editors:

Mazuski C. The Role of VIP SCN Neurons in Circadian Physiology and Behavior. [Doctoral Dissertation]. Washington University in St. Louis; 2017. Available from: https://openscholarship.wustl.edu/art_sci_etds/1233

Washington University in St. Louis

28. Laumann, Timothy. Functional Brain Organization in Space and Time.

Degree: PhD, Biology & Biomedical Sciences (Neurosciences), 2017, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/1122

► The brain is a network functionally organized at many spatial and temporal scales. To understand how the brain processes information, controls behavior and dynamically adapts… (more)

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Laumann, T. (2017). Functional Brain Organization in Space and Time. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/1122

Chicago Manual of Style (16^th Edition):

Laumann, Timothy. “Functional Brain Organization in Space and Time.” 2017. Doctoral Dissertation, Washington University in St. Louis. Accessed March 07, 2021. https://openscholarship.wustl.edu/art_sci_etds/1122.

MLA Handbook (7^th Edition):

Laumann, Timothy. “Functional Brain Organization in Space and Time.” 2017. Web. 07 Mar 2021.

Vancouver:

Laumann T. Functional Brain Organization in Space and Time. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2017. [cited 2021 Mar 07]. Available from: https://openscholarship.wustl.edu/art_sci_etds/1122.

Council of Science Editors:

Laumann T. Functional Brain Organization in Space and Time. [Doctoral Dissertation]. Washington University in St. Louis; 2017. Available from: https://openscholarship.wustl.edu/art_sci_etds/1122

Washington University in St. Louis

29. Cheng, Cheng. A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder.

Degree: PhD, Biology & Biomedical Sciences (Developmental, Regenerative, & Stem Cell Biology), 2018, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/1690

► ABSTRACT OF THE DISSERTATION A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder By Cheng Cheng Doctor of Philosophy… (more)

▼ ABSTRACT OF THE DISSERTATION A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder By Cheng Cheng Doctor of Philosophy in Biology and Biomedical Sciences Developmental, Regenerative and Stem Cell Biology Washington University in St. Louis, 2018 Dr. Azad Bonni, Chair Intellectual disability (ID) is a prevalent neurodevelopmental disorder that affects 1% to 3% of the general population. ID is characterized by developmental deficiencies in cognitive function and adaptive behaviors. Lacking effective treatments, ID currently presents an immense burden to affected families and the economy. Therefore, there is an urgent need to elucidate the pathogenesis of ID. Human genetic studies have associated ID with a number of gene mutations. ID can be divided into two major groups: a non-syndromic form, characterized by intellectual impairment manifesting alone, and a syndromic form, characterized by both cognitive deficiencies and other anomalies, including biochemical disorders, skeletal abnormalities, facial dysmorphisms and neurological disorders. However, scientists have limited their studies to relatively few syndromic forms of ID, such as Rett, Angelman and Fragile X syndrome. In addition to these commonly studied syndromes, Börjeson-Forssman-Lehman syndrome (BFLS) was identified over five decades ago as a cause of X-linked ID and characterized as a syndromic form of moderately to severely impaired cognitive function associated with early developmental delay, truncal obesity, small genitalia, facial dysmorphism and seizures. Whether BFLS patients display other neurological manifestations besides cognitive impairment and seizures remains unexplored. In particular, whereas some genetic forms of ID are accompanied by manifestations of autism spectrum disorders (ASD), whether BFLS also features symptoms and signs of ASD is unknown. Forty years after the first description of BFLS, mutations in the gene encoding plant homeofinger protein 6 (PHF6) were discovered to be causative for BFLS. These mutations are distributed throughout the entire gene in distinct domains of PHF6, and are composed of missense, nonsense, truncation, duplication and frameshift. Accumulating evidence suggests that PHF6 plays a role in transcriptional regulation. PHF6 contains nuclear localization sequences and PHD domains and can interact with transcriptional elongation complex, PAF1 to regulate cortical neural migration. Furthermore, other studies also suggest that PHF6 may regulate transcription through association with the nucleosome remodeling complex NuRD and upstream binding factor UBF1. The discovery of PHF6 interactors and their functions during neural development have raised additional interesting questions in understanding BFLS pathogenesis. How does PHF6 regulation of gene expression at the genome-wide level impact BFLS pathogenesis? How do specific PHF6 mutations trigger the pathogenesis of BFLS? Within this thesis, I provide detailed… Advisors/Committee Members: Azad Bonni, Joseph Dougherty, Andrew Yoo, Harrison Gabel, Jason Yi.

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cheng, C. (2018). A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/1690

Chicago Manual of Style (16^th Edition):

Cheng, Cheng. “A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder.” 2018. Doctoral Dissertation, Washington University in St. Louis. Accessed March 07, 2021. https://openscholarship.wustl.edu/art_sci_etds/1690.

MLA Handbook (7^th Edition):

Cheng, Cheng. “A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder.” 2018. Web. 07 Mar 2021.

Vancouver:

Cheng C. A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2018. [cited 2021 Mar 07]. Available from: https://openscholarship.wustl.edu/art_sci_etds/1690.

Council of Science Editors:

Cheng C. A Mouse Model of Börjeson-Forssman-Lehmann Syndrome reveals a potential link with Autism Spectrum Disorder. [Doctoral Dissertation]. Washington University in St. Louis; 2018. Available from: https://openscholarship.wustl.edu/art_sci_etds/1690

Washington University in St. Louis

30. Liang, Xitong. Neural Mechanisms of Drosophila Circadian Rhythms.

Degree: PhD, Biology & Biomedical Sciences (Neurosciences), 2018, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/1707

► Animals show circadian rhythms in a variety of physiological functions and behaviors. In Drosophila melanogaster, behavioral rhythms are driven by circadian clock genes that… (more)

▼ Animals show circadian rhythms in a variety of physiological functions and behaviors. In Drosophila melanogaster, behavioral rhythms are driven by circadian clock genes that are oscillating in ~150 circadian pacemaker neurons. To explain how circadian neurons encode time and regulate different behavioral rhythms, I performed 24-hour in vivo whole-brain calcium imaging using light-sheet microscopy. First, I found that different groups of circadian neurons show circadian rhythms in spontaneous neural activity with diverse phases. The neural activity phases of the M and E pacemaker groups, which are associated with the morning and evening locomotor activities respectively, occur ~4 hours before their respective behaviors. I also showed that neural activity rhythms are generated by circadian clock gene oscillations, which regulate the expression of IP3R and T-type calcium channels. Next, I asked how the diverse phases of neural activity are generated from the in-phase clock gene oscillations. Groups of circadian neurons inhibit each other via long-duration neuromodulation, mediated by neuropeptides PDF and sNPF, such that their activity phases are properly staggered across the day and night. Certain activity phases are also regulated by environmental light inputs. I then identified an output pathway by which circadian neurons regulate the locomotor activity rhythm. M and E pacemaker groups independently activate a common pre-motor center (termed ellipsoid body ring neurons) through the agency of specific dopaminergic interneurons. Finally, using methods including whole-brain pan-neuronal imaging, I further identified several output circuits downstream of circadian neurons. Circadian neural activity rhythms propagate through these circuits to regulate different behavioral outputs including sleep, olfaction, mating, and feeding rhythms. Together, my findings show how circadian clocks regulate diverse behavioral outputs by two steps; first, circadian clock genes generate diverse circadian neural activity rhythms within a network of interacting pacemaker neurons; then, sequentially-active pacemaker neurons independently and together regulate diverse behavioral outputs by generating diverse circadian neural activity rhythms in different downstream output circuits. Advisors/Committee Members: Paul Timothy H. Taghert Holy, Martha Bagnall, Erik Herzog, Daniel Kerschensteiner.

Subjects/Keywords: Neuroscience and Neurobiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Liang, X. (2018). Neural Mechanisms of Drosophila Circadian Rhythms. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/1707

Chicago Manual of Style (16^th Edition):

Liang, Xitong. “Neural Mechanisms of Drosophila Circadian Rhythms.” 2018. Doctoral Dissertation, Washington University in St. Louis. Accessed March 07, 2021. https://openscholarship.wustl.edu/art_sci_etds/1707.

MLA Handbook (7^th Edition):

Liang, Xitong. “Neural Mechanisms of Drosophila Circadian Rhythms.” 2018. Web. 07 Mar 2021.

Vancouver:

Liang X. Neural Mechanisms of Drosophila Circadian Rhythms. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2018. [cited 2021 Mar 07]. Available from: https://openscholarship.wustl.edu/art_sci_etds/1707.

Council of Science Editors:

Liang X. Neural Mechanisms of Drosophila Circadian Rhythms. [Doctoral Dissertation]. Washington University in St. Louis; 2018. Available from: https://openscholarship.wustl.edu/art_sci_etds/1707

Open Access Theses and Dissertations