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 October 17, 2019. https://ir.uiowa.edu/etd/1811.

MLA Handbook (7^th Edition):

Yin, Terry. “Neuroprotective strategies for traumatic brain injury.” 2015. Web. 17 Oct 2019.

Vancouver:

Yin T. Neuroprotective strategies for traumatic brain injury. [Internet] [Doctoral dissertation]. University of Iowa; 2015. [cited 2019 Oct 17]. 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

Texas Medical Center

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

Degree: PhD, 2014, Texas Medical Center

URL: http://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 http://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 October 17, 2019. http://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. 17 Oct 2019.

Vancouver:

Eagleman, Sarah PD. EFFECTS OF RESTING STATE ON PERCEPTUAL LEARNING. [Internet] [Doctoral dissertation]. Texas Medical Center; 2014. [cited 2019 Oct 17]. Available from: http://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: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/432

3. Abbott, Brendan. Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression.

Degree: 2018, University of Massachusetts

URL: https://scholarworks.umass.edu/masters_theses_2/625

► Depression and related disorders are characterized by motivational dysfunctions, including deficits in behavioral activation and exertion of effort. Animal models of relevance to depression… (more)

▼ Depression and related disorders are characterized by motivational dysfunctions, including deficits in behavioral activation and exertion of effort. Animal models of relevance to depression represent a critical starting point in elucidating the neurobiological mechanisms underlying motivational dysfunctions. The present study explored the use of the Wistar-Kyoto (WKY) animal model of depression to examine effort-related functions as measured by voluntary wheel running and performance on a mixed fixed ratio 5/progressive ratio (FR5/PR) operant task. Given the known link between activational aspects of motivation and the mesocorticolimbic dopamine (DA) system, the behavioral effects of d-amphetamine (0.5 and 1.0 mg/kg, IP), a psychostimulant that increases DA release, were evaluated in WKY and control Sprague-Dawley (SD) male and female rats responding on a mixed FR5/PR task. An additional experiment assessed intracellular content of monoamine neurotransmitters and their metabolites in relevant mesocorticolimbic brain regions, including the medial prefrontal cortex, the nucleus accumbens and the ventrolateral striatum using HPLC-ED. WKY rats demonstrated initial effort-related deficits in FR5/PR responding compared to SD controls, which ameliorated with training. Amphetamine significantly decreased FR5 work output, but increased responding on the PR phase in both SD and WKY rats. This effect was more pronounced in SD rats compare to WKY rats. In addition, sex differences were evident both in FR5/PR performance and in the behavioral response to amphetamine treatment. Moreover, females demonstrated higher levels of voluntary wheel-running than males. Finally, tissue concentrations of dopamine were lower in the NA and VLS of WKY compared to SD rats. Taken together, results suggest dysfunctions in mesolimbic DA neurotransmission in the WKY strain, likely underlying the depressive phenotype. The present study represents an important initial step in validating the WKY strain as a rat model of effort-related dysfunctions relevant to depression and other neuropsychiatric disorders. Advisors/Committee Members: Mariana Pereira, Andrew Farrar.

Subjects/Keywords: depression; dopamine; effort; motivation; serotonin; rodent; Behavioral Neurobiology; Biological Psychology; Cognitive Neuroscience; Molecular and Cellular Neuroscience; Other Neuroscience and Neurobiology; Other Psychology; Pharmacology; Systems Neuroscience

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APA (6^th Edition):

Abbott, B. (2018). Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression. (Thesis). University of Massachusetts. Retrieved from https://scholarworks.umass.edu/masters_theses_2/625

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):

Abbott, Brendan. “Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression.” 2018. Thesis, University of Massachusetts. Accessed October 17, 2019. https://scholarworks.umass.edu/masters_theses_2/625.

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

MLA Handbook (7^th Edition):

Abbott, Brendan. “Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression.” 2018. Web. 17 Oct 2019.

Vancouver:

Abbott B. Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression. [Internet] [Thesis]. University of Massachusetts; 2018. [cited 2019 Oct 17]. Available from: https://scholarworks.umass.edu/masters_theses_2/625.

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

Council of Science Editors:

Abbott B. Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression. [Thesis]. University of Massachusetts; 2018. Available from: https://scholarworks.umass.edu/masters_theses_2/625

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

University of Wisconsin – Milwaukee

4. Pullins, Shane E. Rescuing Age-related Proteolysis Deficits with Methylene Blue.

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

URL: https://dc.uwm.edu/etd/1679

► The average lifespan is constantly increasing with the advent of new medical techniques, and age-related cognitive decline is becoming a prevalent societal issue. Even… (more)

Subjects/Keywords: Aging; Memory; Methylene Blue; Proteasome; Neuroscience and Neurobiology; Other Psychology

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APA (6^th Edition):

Pullins, S. E. (2017). Rescuing Age-related Proteolysis Deficits with Methylene Blue. (Thesis). University of Wisconsin – Milwaukee. Retrieved from https://dc.uwm.edu/etd/1679

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):

Pullins, Shane E. “Rescuing Age-related Proteolysis Deficits with Methylene Blue.” 2017. Thesis, University of Wisconsin – Milwaukee. Accessed October 17, 2019. https://dc.uwm.edu/etd/1679.

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

MLA Handbook (7^th Edition):

Pullins, Shane E. “Rescuing Age-related Proteolysis Deficits with Methylene Blue.” 2017. Web. 17 Oct 2019.

Vancouver:

Pullins SE. Rescuing Age-related Proteolysis Deficits with Methylene Blue. [Internet] [Thesis]. University of Wisconsin – Milwaukee; 2017. [cited 2019 Oct 17]. Available from: https://dc.uwm.edu/etd/1679.

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

Council of Science Editors:

Pullins SE. Rescuing Age-related Proteolysis Deficits with Methylene Blue. [Thesis]. University of Wisconsin – Milwaukee; 2017. Available from: https://dc.uwm.edu/etd/1679

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

University of Pennsylvania

5. Lindl, Kathryn A. Activation of the Integrated Stress Response in HIV-Associated Neurocognitive Disorder.

Degree: 2010, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/276

► HIV-associated neurocognitive disorders (HAND) are comprised of a host of behavioral, cognitive, and motor disabilities and can range from more minor disorders that largely allow… (more)

▼ HIV-associated neurocognitive disorders (HAND) are comprised of a host of behavioral, cognitive, and motor disabilities and can range from more minor disorders that largely allow basic daily functioning to severe disorders, such as HIV-associated dementia. The mechanisms that ultimately result in neuronal death in HAND are not known. Presented here are data demonstrating activation of the Integrated Stress Response (ISR) in cortical autopsy tissue from HAND patients, as well as data characterizing the nature of the activation of this cellular stress response in this disease. Specifically, we have shown that there are increased levels of the molecular chaperone protein, BiP, which serves as an indicator of general ISR activation. We then present data to suggest that, of the three prongs of the ISR, the prong initiated by ATF6 appears to be active, while PERK does not appear to initiate the prong it regulates. However, intriguingly, proteins downstream of PERK, namely global pEIF2α and astrocytic ATF4 do appear to be activated, suggesting that other initiators outside of the PERK pathway may be acting on these classic components of the ISR. Finally, we show data suggesting that Nrf2, the master regulator of the endogenous antioxidant component of the ISR, may be active in the cortex of HAND patients. While the ISR is clearly a protective response, able to help individual cells protect themselves from toxic insults, it is also able to initiate cellular apoptosis, which in principle protects healthy cells from a dangerous necrotic death of neighboring cells. However, under conditions of chronic stress in the CNS, such as that seen in HAND, too many neurons may die as a result of ISR-initiated apoptosis, thereby resulting in the neurocognitive decline with which these patients are afflicted. Thus, the findings presented here provide starting points of investigation for research aimed at developing potential therapeutic targets for HAND, with some targets for which their response must be increased by therapies and other targets for which their response must be dampened by therapies.

Subjects/Keywords: unfolded protein response; ER stress response; 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):

Lindl, K. A. (2010). Activation of the Integrated Stress Response in HIV-Associated Neurocognitive Disorder. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/276

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):

Lindl, Kathryn A. “Activation of the Integrated Stress Response in HIV-Associated Neurocognitive Disorder.” 2010. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/276.

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

MLA Handbook (7^th Edition):

Lindl, Kathryn A. “Activation of the Integrated Stress Response in HIV-Associated Neurocognitive Disorder.” 2010. Web. 17 Oct 2019.

Vancouver:

Lindl KA. Activation of the Integrated Stress Response in HIV-Associated Neurocognitive Disorder. [Internet] [Thesis]. University of Pennsylvania; 2010. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/276.

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

Council of Science Editors:

Lindl KA. Activation of the Integrated Stress Response in HIV-Associated Neurocognitive Disorder. [Thesis]. University of Pennsylvania; 2010. Available from: https://repository.upenn.edu/edissertations/276

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

University of Pennsylvania

6. Hughes, Ethan G. Mechanisms of Synapse formation and Maintenance: Insights From the Developing and Diseased Nervous System.

Degree: 2009, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/25

► ABSTRACT MECHANISMS OF SYNAPSE FORMATION AND MAINTENANCE: INSIGHTS FROM THE DEVELOPING AND DISEASED NERVOUS SYSTEM Ethan G. Hughes Rita J. Balice-Gordon, Ph.D. The formation and… (more)

▼ ABSTRACT MECHANISMS OF SYNAPSE FORMATION AND MAINTENANCE: INSIGHTS FROM THE DEVELOPING AND DISEASED NERVOUS SYSTEM Ethan G. Hughes Rita J. Balice-Gordon, Ph.D. The formation and maintenance of synapses is essential for the central nervous system (CNS) to function. In the developing nervous system, the assembly of synaptic circuits is a complex and dynamic process, requiring the coordinated exchange of signals between pre- and postsynaptic neurons and surrounding glia. The maintenance and modulation of synaptic connections is required for normal CNS function and ongoing plasticity. The structural and functional integrity of synaptic connections is often modified or lost in the diseased nervous system, resulting in profound cognitive and behavioral deficits. While some aspects of the mechanisms underlying the formation, maintenance and plasticity of CNS synapses in the developing and diseased nervous system have been elucidated, many more remain to be understood. In my thesis work, I have examined the role of astrocytes in the development of GABAergic hippocampal synapses in in vitro models. I have also examined the maintenance of glutamatergic synapses in in vitro and in vivo models of anti-NMDAR encephalitis, an immune-mediated disorder of memory and behavior. First, I demonstrate that secreted factors released from astrocytes specifically increase GABAergic axon length, branching, and synaptogenesis, that these effects are not mediated by several well-known candidates, and that the secreted factors from astrocytes are proteins. Second, I examined the identity of the proteins released from astrocytes that affect GABAergic neurons using size fractionation, mass spectroscopy, and computational analyses. Third, I examined the cellular and synaptic mechanisms underlying anti-NMDAR encephalitis and investigated the effects of autoantibodies from patients with this disorder on the maintenance and function of CNS excitatory synapses. Together, my work extends our understanding of how neuron-glial communication modulates the formation of synapses in the developing brain, and how the disruption of synapse maintenance may underlie cognitive deficits in the diseased nervous system.

Subjects/Keywords: Astrocyte; inhibitory neuron; synaptogenesis; Autoimmune; encephalitis; NMDA receptor; Developmental Neuroscience; Other Neuroscience and Neurobiology

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APA (6^th Edition):

Hughes, E. G. (2009). Mechanisms of Synapse formation and Maintenance: Insights From the Developing and Diseased Nervous System. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/25

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):

Hughes, Ethan G. “Mechanisms of Synapse formation and Maintenance: Insights From the Developing and Diseased Nervous System.” 2009. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/25.

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

MLA Handbook (7^th Edition):

Hughes, Ethan G. “Mechanisms of Synapse formation and Maintenance: Insights From the Developing and Diseased Nervous System.” 2009. Web. 17 Oct 2019.

Vancouver:

Hughes EG. Mechanisms of Synapse formation and Maintenance: Insights From the Developing and Diseased Nervous System. [Internet] [Thesis]. University of Pennsylvania; 2009. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/25.

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

Council of Science Editors:

Hughes EG. Mechanisms of Synapse formation and Maintenance: Insights From the Developing and Diseased Nervous System. [Thesis]. University of Pennsylvania; 2009. Available from: https://repository.upenn.edu/edissertations/25

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

7. Ginder, Darren Earl. Improving dopamine monitoring with NCAM and the effects of intranasal oxytocin on dopamine signaling in the rat brain.

Degree: MS, Biology, 2019, Eastern Washington University

URL: https://dc.ewu.edu/theses/555

► Dopamine (DA) is a neurohormone highly involved in learning and memory. Oxytocin (OXT), another neurohormone, has also been implicated in learning and memory. Fast-scan… (more)

Subjects/Keywords: Hormones, Hormone Substitutes, and Hormone Antagonists; Molecular and Cellular Neuroscience; Other Neuroscience and Neurobiology

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APA (6^th Edition):

Ginder, D. E. (2019). Improving dopamine monitoring with NCAM and the effects of intranasal oxytocin on dopamine signaling in the rat brain. (Thesis). Eastern Washington University. Retrieved from https://dc.ewu.edu/theses/555

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):

Ginder, Darren Earl. “Improving dopamine monitoring with NCAM and the effects of intranasal oxytocin on dopamine signaling in the rat brain.” 2019. Thesis, Eastern Washington University. Accessed October 17, 2019. https://dc.ewu.edu/theses/555.

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

MLA Handbook (7^th Edition):

Ginder, Darren Earl. “Improving dopamine monitoring with NCAM and the effects of intranasal oxytocin on dopamine signaling in the rat brain.” 2019. Web. 17 Oct 2019.

Vancouver:

Ginder DE. Improving dopamine monitoring with NCAM and the effects of intranasal oxytocin on dopamine signaling in the rat brain. [Internet] [Thesis]. Eastern Washington University; 2019. [cited 2019 Oct 17]. Available from: https://dc.ewu.edu/theses/555.

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

Council of Science Editors:

Ginder DE. Improving dopamine monitoring with NCAM and the effects of intranasal oxytocin on dopamine signaling in the rat brain. [Thesis]. Eastern Washington University; 2019. Available from: https://dc.ewu.edu/theses/555

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

Texas Medical Center

8. Liu, Wei-Li. DIRECT INPUTS TO OFF Α AND G9 GANGLION CELLS FROM AII AMACRINE CELLS IN RABBIT RETINA.

Degree: MS, 2010, Texas Medical Center

URL: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/81

► In the mammalian retina, AII amacrine cells are essential in the rod pathway for dark-adapted vision. But they also have a “day job”, to provide… (more)

Subjects/Keywords: retina; rabbit; AII; Crossover inhibition; OFF alpha; cell classification; Cells; 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):

Liu, W. (2010). DIRECT INPUTS TO OFF Α AND G9 GANGLION CELLS FROM AII AMACRINE CELLS IN RABBIT RETINA. (Masters Thesis). Texas Medical Center. Retrieved from http://digitalcommons.library.tmc.edu/utgsbs_dissertations/81

Chicago Manual of Style (16^th Edition):

Liu, Wei-Li. “DIRECT INPUTS TO OFF Α AND G9 GANGLION CELLS FROM AII AMACRINE CELLS IN RABBIT RETINA.” 2010. Masters Thesis, Texas Medical Center. Accessed October 17, 2019. http://digitalcommons.library.tmc.edu/utgsbs_dissertations/81.

MLA Handbook (7^th Edition):

Liu, Wei-Li. “DIRECT INPUTS TO OFF Α AND G9 GANGLION CELLS FROM AII AMACRINE CELLS IN RABBIT RETINA.” 2010. Web. 17 Oct 2019.

Vancouver:

Liu W. DIRECT INPUTS TO OFF Α AND G9 GANGLION CELLS FROM AII AMACRINE CELLS IN RABBIT RETINA. [Internet] [Masters thesis]. Texas Medical Center; 2010. [cited 2019 Oct 17]. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/81.

Council of Science Editors:

Liu W. DIRECT INPUTS TO OFF Α AND G9 GANGLION CELLS FROM AII AMACRINE CELLS IN RABBIT RETINA. [Masters Thesis]. Texas Medical Center; 2010. Available from: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/81

Texas Medical Center

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

Degree: PhD, 2014, Texas Medical Center

URL: http://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 http://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 October 17, 2019. http://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. 17 Oct 2019.

Vancouver:

Robinson CR. Mechanisms of Astrocyte Contribution to Bortezomib-Induced Peripheral Neuropathy. [Internet] [Doctoral dissertation]. Texas Medical Center; 2014. [cited 2019 Oct 17]. Available from: http://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: http://digitalcommons.library.tmc.edu/utgsbs_dissertations/485

University of Kentucky

10. 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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Sethi M. SLEEP ALTERATIONS IN MOUSE GENETIC MODELS OF HUMAN DISEASE. [Internet] [Doctoral dissertation]. University of Kentucky; 2016. [cited 2019 Oct 17]. 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

11. 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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Compton C. The fatigue-associated changes in estimates of persistent inward current in human motor neurons. [Internet] [Thesis]. Wilfrid Laurier University; 2018. [cited 2019 Oct 17]. 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

12. 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… (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 (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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Richardson BP. Electrophysiological and Behavioral Working Memory Differences Between Musicians and Non-Musicians. [Internet] [Masters thesis]. Central Washington University; 2015. [cited 2019 Oct 17]. 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

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

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 October 17, 2019. 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. 17 Oct 2019.

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 2019 Oct 17]. 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

University of Maine

14. Hennings, Maxwell A. An Analysis of Neurogenesis in a Mouse Model of Chemotherapy Related Cognitive Impairment.

Degree: PhD, Psychology, 2017, University of Maine

URL: https://digitalcommons.library.umaine.edu/etd/2648

► Cancer patients treated with adjuvant chemotherapy often experience cognitive decline following treatment. This phenomenon, often dubbed “chemo brain” or “chemo fog” is usually temporary,… (more)

▼ Cancer patients treated with adjuvant chemotherapy often experience cognitive decline following treatment. This phenomenon, often dubbed “chemo brain” or “chemo fog” is usually temporary, but for a subset of survivors, these cognitive impairments can be long-lasting (>10 years) and negatively affect patients’ quality of life, career performance, and social fulfillment. While it is unclear what neurobiological mechanisms underlie chemotherapy related cognitive impairment, the majority of the animal literature has focused on adult neurogenesis. One process important for neurogenesis is the proliferation of new neurons within the dentate gyrus of the hippocampus. It is evident that many chemotherapy agents can negatively impact levels of neurogenesis shortly after treatment. However, only a few studies have investigated the long-term impact of chemotherapy on neurogenesis. The present studies explore the long-term impact of three commonly used chemotherapy agents on neurogenesis utilizing immunohistochemistry in a male C57BL/6J mouse model. EXP 1: The effects of cyclophosphamide or doxorubicin on neuronal proliferation were evaluated at 1 day, 56 days and 6 months post-treatment. Results indicated that neither cyclophosphamide nor doxorubicin treatment altered proliferation rates across either short-term or long-term intervals. EXP 2: The effects of 5-FU (alone or in combination with either the antioxidant melatonin or the antidepressant fluoxetine) on neuronal proliferation were evaluated at 1 day, 56 days and 6 months post-treatment. The results indicated that there was no effect of 5-FU or neuroprotectant treatment at any time point. The current studies suggest that neither cyclophosphamide, doxorubicin, nor 5-FU affect neurogenic proliferation in C57BL/6J mice directly after injection or up to 6 months post injection. As such, impaired neurogenic proliferation is an unlikely cellular mechanism for chemotherapy related cognitive impairment detected within this strain. Advisors/Committee Members: Thane E. Fremouw, Shawn W. Ell, Marie J. Hayes.

Subjects/Keywords: Chemotherapy; Neurogenesis; Chemotherapy related cognitive impairment; Mice; Neuroscience; Chemobrain; Animals; Behavioral Neurobiology; Biological Factors; Biological Psychology; Cognitive Neuroscience; Life Sciences; Mental Disorders; Molecular and Cellular Neuroscience; Neuroscience and Neurobiology; Other Chemicals and Drugs; Other Neuroscience and Neurobiology; Psychology

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APA (6^th Edition):

Hennings, M. A. (2017). An Analysis of Neurogenesis in a Mouse Model of Chemotherapy Related Cognitive Impairment. (Doctoral Dissertation). University of Maine. Retrieved from https://digitalcommons.library.umaine.edu/etd/2648

Chicago Manual of Style (16^th Edition):

Hennings, Maxwell A. “An Analysis of Neurogenesis in a Mouse Model of Chemotherapy Related Cognitive Impairment.” 2017. Doctoral Dissertation, University of Maine. Accessed October 17, 2019. https://digitalcommons.library.umaine.edu/etd/2648.

MLA Handbook (7^th Edition):

Hennings, Maxwell A. “An Analysis of Neurogenesis in a Mouse Model of Chemotherapy Related Cognitive Impairment.” 2017. Web. 17 Oct 2019.

Vancouver:

Hennings MA. An Analysis of Neurogenesis in a Mouse Model of Chemotherapy Related Cognitive Impairment. [Internet] [Doctoral dissertation]. University of Maine; 2017. [cited 2019 Oct 17]. Available from: https://digitalcommons.library.umaine.edu/etd/2648.

Council of Science Editors:

Hennings MA. An Analysis of Neurogenesis in a Mouse Model of Chemotherapy Related Cognitive Impairment. [Doctoral Dissertation]. University of Maine; 2017. Available from: https://digitalcommons.library.umaine.edu/etd/2648

McMaster University

15. Guest, Kelly A. Investigating the Role of Synapsin II in Neurological Disorders Involving Dysregulated Dopaminergic Transmission.

Degree: MS, 2010, McMaster University

URL: http://hdl.handle.net/11375/12274

►

Schizophrenia (SCZ) is a debilitating mental illness that affects roughly I % of the world's population. Current theories about the etiology of this disease… (more)

▼

Schizophrenia (SCZ) is a debilitating mental illness that affects roughly I % of the world's population. Current theories about the etiology of this disease highlight dismptions in dopamine (DA) and glutamate. However, a more recent theory, the 'synaptic hypothesis' proposes that the fundamental pathology of this illness involves disruptions in synaptic transmission. The synapsins are a family of neuron specific phosphoproteins that play an important role in neurotransmitter release, synapse formation and maintaining a reserve pool of synaptic vesicles. Previous research has suggested that synapsin II has a role in the etiology of SCZ. For example, synapsin II mRNA is significantly reduced in the medial prefrontal cortex (MPFC) of patients, and synapsin II knockout rats display a variety of behavioural abnormalities which mimic human SCZ. Considering that SCZ may result from changes at the synapse, we wanted to further elucidate the role of synapsin Il by measuring protein expression in post-mortem PFC samples. Overall, our results revealed that synapsin Ira and lIb are not significantly different betv,Ieen patients and controls, however, we hypothesize that synapsin Il expression has been nOlmalized in patients due to antipsychotic drug (APD) use. In fact, we discovered that treatment with atypical APDs significantly increases synapsin Il in the prefrontal cortex (PFC) of patients, which may underlie the beneficial effects of these dmgs. Another objective of our work was to investigate the expression of various presynaptic proteins in post-mortem samples from patients with Parkinson's disease (PD). Parkinson's disease, like SCZ, is an illness which involves dysregulated dopaminergic transmission and synaptic dysfunction. Therefore, we hypothesized that synapsin II might also be disrupted in patients with PD. Our results demonstrated that synapsin IIa and lIb are significantly reduced in the substantia nigra (SN), but not the striatum (STR) or PFC of patients, when compared to controls. Further, no changes were observed in the other synapsins (I or III), or synaptophysin, which suggests that synapsin II dysregulation may be specific to disorders which involve disruptions in dopamine (DA).

Master of Science (MS)

Advisors/Committee Members: Mishra, R.K., Neurosciences.

Subjects/Keywords: Neuroscience and Neurobiology; Neuroscience and Neurobiology

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APA (6^th Edition):

Guest, K. A. (2010). Investigating the Role of Synapsin II in Neurological Disorders Involving Dysregulated Dopaminergic Transmission. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/12274

Chicago Manual of Style (16^th Edition):

Guest, Kelly A. “Investigating the Role of Synapsin II in Neurological Disorders Involving Dysregulated Dopaminergic Transmission.” 2010. Masters Thesis, McMaster University. Accessed October 17, 2019. http://hdl.handle.net/11375/12274.

MLA Handbook (7^th Edition):

Guest, Kelly A. “Investigating the Role of Synapsin II in Neurological Disorders Involving Dysregulated Dopaminergic Transmission.” 2010. Web. 17 Oct 2019.

Vancouver:

Guest KA. Investigating the Role of Synapsin II in Neurological Disorders Involving Dysregulated Dopaminergic Transmission. [Internet] [Masters thesis]. McMaster University; 2010. [cited 2019 Oct 17]. Available from: http://hdl.handle.net/11375/12274.

Council of Science Editors:

Guest KA. Investigating the Role of Synapsin II in Neurological Disorders Involving Dysregulated Dopaminergic Transmission. [Masters Thesis]. McMaster University; 2010. Available from: http://hdl.handle.net/11375/12274

University of Vermont

16. 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 October 17, 2019. 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. 17 Oct 2019.

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 2019 Oct 17]. 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 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 (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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Spohn SN. Protective Actions of 5-HT4 Receptors in the Colonic Epithelium. [Internet] [Doctoral dissertation]. University of Vermont; 2016. [cited 2019 Oct 17]. 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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Pappas AC. Impact of Subarachnoid Hemorrhage on Astrocyte Calcium Signaling: Implications for Impaired Neurovascular Coupling. [Internet] [Doctoral dissertation]. University of Vermont; 2016. [cited 2019 Oct 17]. 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

Carnegie Mellon University

19. 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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Wen J. Experience-dependent plasticity of layer 2/3 circuits in developing somatosensory neocortex. [Internet] [Thesis]. Carnegie Mellon University; 2012. [cited 2019 Oct 17]. 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

Washington University in St. Louis

20. 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 (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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Mazuski C. The Role of VIP SCN Neurons in Circadian Physiology and Behavior. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2017. [cited 2019 Oct 17]. 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

21. 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 (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 October 17, 2019. 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. 17 Oct 2019.

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 2019 Oct 17]. 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

Loyola University Chicago

22. 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 (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 October 17, 2019. 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. 17 Oct 2019.

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 2019 Oct 17]. 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

23. 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: http://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 http://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 October 17, 2019. http://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. 17 Oct 2019.

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 2019 Oct 17]. Available from: http://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: http://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 Pennsylvania

24. 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 October 17, 2019. 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. 17 Oct 2019.

Vancouver:

Boccitto M. Genetic and Pharmacological Approaches to Preventing Neurodegeneration. [Internet] [Thesis]. University of Pennsylvania; 2012. [cited 2019 Oct 17]. 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

University of Pennsylvania

25. Ozek, Ceren. Regional Roles of Central Trkb Receptors in Energy Balance and Regulation by Ptp1b.

Degree: 2015, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1927

► Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed phosphatase implicated in energy balance regulation. CNS-specific PTP1B-deficiency results in a lean phenotype with resistance to… (more)

▼ Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed phosphatase implicated in energy balance regulation. CNS-specific PTP1B-deficiency results in a lean phenotype with resistance to diet-induced obesity. PTP1B antagonizes actions of leptin, which regulates central energy balance by suppressing food intake and elevating energy expenditure. Although the metabolic effects of PTP1B-deficiency have been largely attributed to improved leptin sensitivity, mice lacking both leptin and PTP1B weigh less compared to the mice lacking leptin only, suggesting leptin-independent metabolic effects of PTP1B-deficiency. Biochemical studies have identified tropomyosin receptor kinase B (TrkB) as a potential substrate for PTP1B. Since TrkB ligand brain-derived neurotrophic factor (BDNF) is a key player in energy balance, this dissertation tests the hypothesis that PTP1B is a physiological regulator of central BDNF/TrkB signaling and further examines the metabolic role of endogenous hypothalamic and hindbrain BDNF/TrkB signaling. To assess whether PTP1B is a physiological regulator of central BDNF/TrkB signaling, an immortalized human neuronal SH-SY5Y-TrkB cell line was utilized in biochemical studies in vitro, and a mouse model of global PTP1B-deficiency (Ptpn1-/-) was used to test the metabolic response to exogenous central BDNF delivery in vivo. In SH-SY5Y-TrkB cells, PTP1B overexpression and PTP1B inhibition impairs and augments TrkB signaling, respectively. Furthermore, PTP1B interacts with the BDNF-activated TrkB receptor. Ptpn1-/- mice exhibit enhanced hypothalamic TrkB phosphorylation, and are hypersensitive to central BDNF-induced increase in core temperature. Whether Ptpn1-/- mice show increased hypothalamic neurogenesis was explored through BrdU studies. To further elucidate the role of endogenous BDNF/TrkB signaling in central metabolic control, hypothalamus (Nkx2.1-Ntrk2-/-) or hindbrain (Phox2b-Ntrk2+/-) specific TrkB-deficient mice were generated and their metabolic phenotype was analyzed in comparison to wild type controls. Nkx2.1-Ntrk2-/- mice display increased body weight and adiposity due to alterations in food intake and energy expenditure, and have glucose homeostasis impairments. Interestingly, female mice lacking TrkB in the hypothalamus have a more robust metabolic phenotype. Phox2b-Ntrk2+/- mice exhibit pronounced hyperphagia despite the absence of a body weight phenotype. In summary, these data clearly establish PTP1B as a novel, physiological regulator of central BDNF/TrkB signaling, and that endogenous hypothalamic and hindbrain TrkB signaling are essential to central metabolic control.

Subjects/Keywords: Neuroscience and Neurobiology

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APA (6^th Edition):

Ozek, C. (2015). Regional Roles of Central Trkb Receptors in Energy Balance and Regulation by Ptp1b. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1927

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):

Ozek, Ceren. “Regional Roles of Central Trkb Receptors in Energy Balance and Regulation by Ptp1b.” 2015. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/1927.

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

MLA Handbook (7^th Edition):

Ozek, Ceren. “Regional Roles of Central Trkb Receptors in Energy Balance and Regulation by Ptp1b.” 2015. Web. 17 Oct 2019.

Vancouver:

Ozek C. Regional Roles of Central Trkb Receptors in Energy Balance and Regulation by Ptp1b. [Internet] [Thesis]. University of Pennsylvania; 2015. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/1927.

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

Council of Science Editors:

Ozek C. Regional Roles of Central Trkb Receptors in Energy Balance and Regulation by Ptp1b. [Thesis]. University of Pennsylvania; 2015. Available from: https://repository.upenn.edu/edissertations/1927

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

University of Pennsylvania

26. Chen, Julie. Novel Viral asnd Astrocytic Contributors to Epilepsy.

Degree: 2015, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1647

► Epilepsy is a neurological seizure disorder affecting approximately 1% of the world’s population. Seizure disorders are numerous, heterogeneous, and can develop from a multitude of… (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):

Chen, J. (2015). Novel Viral asnd Astrocytic Contributors to Epilepsy. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1647

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):

Chen, Julie. “Novel Viral asnd Astrocytic Contributors to Epilepsy.” 2015. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/1647.

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

MLA Handbook (7^th Edition):

Chen, Julie. “Novel Viral asnd Astrocytic Contributors to Epilepsy.” 2015. Web. 17 Oct 2019.

Vancouver:

Chen J. Novel Viral asnd Astrocytic Contributors to Epilepsy. [Internet] [Thesis]. University of Pennsylvania; 2015. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/1647.

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

Council of Science Editors:

Chen J. Novel Viral asnd Astrocytic Contributors to Epilepsy. [Thesis]. University of Pennsylvania; 2015. Available from: https://repository.upenn.edu/edissertations/1647

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

University of Pennsylvania

27. Maguire, Sarah. The "Ins and Outs" of Sleep: How Internal Metabolic and External Environmental Signals Affect the Sleep Process.

Degree: 2014, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1356

► The behavioral pattern of activity followed by rest (activity:rest) is an evolutionarily conserved trait. A prominent manifestation of rest in vertebrates consists of sleep, which… (more)

▼ The behavioral pattern of activity followed by rest (activity:rest) is an evolutionarily conserved trait. A prominent manifestation of rest in vertebrates consists of sleep, which is adaptive because a disruption of sleep by internal or external influences results in severe health outcomes such as obesity, mood disorders, cognitive impairment, and so forth. Despite the clinical imperative to understand how these cues influence sleep, the mechanisms by which they do so are still unclear. Internally, metabolic cues interact with biochemical pathways that regulate sleep amount and quality. Externally, numerous environmental cues such as light, temperature, and chemicals affect the timing of sleep behavior. The goal of this thesis is to understand the mechanisms by which one internal (the `ins') and one external (the `outs') cue regulates sleep behavior using Drosophila melanogaster. This work consists of two independent projects that evaluate the `ins and outs' of sleep. We begin with the `ins' by addressing how one metabolic enzyme GABA Transaminase (GABAT) controls energy and sleep homeostasis. GABAT is a mitochondrial enzyme found in GABAergic neurons and glial cells where it breaks down the sleep-promoting neurotransmitter, GABA, into glutamate and succinic semialdehyde, both of which can also be used for energy via the TCA cycle. In this study, we determine the mechanism by which GABAT regulates metabolic and sleep homeostasis. In our second project, we evaluate the `outs' of sleep by examining an uncharacterized phenomenon whereby organisms lose their ability to maintain the circadian timing of sleep cycles in the presence of cold-temperature stress. In this project, we use wild-derived flies to evaluate the evolutionary significance of maintaining circadian cycles in some strains regardless of temperature variance, and then determine the cellular and molecular mechanism by which other strains lose their ability to drive circadian rhythms of behavior at low temperature. Overall, the work accomplished in this thesis puts us one step closer towards understanding the `ins and outs' of sleep.

Subjects/Keywords: Neuroscience and Neurobiology

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

APA (6^th Edition):

Maguire, S. (2014). The "Ins and Outs" of Sleep: How Internal Metabolic and External Environmental Signals Affect the Sleep Process. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1356

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):

Maguire, Sarah. “The "Ins and Outs" of Sleep: How Internal Metabolic and External Environmental Signals Affect the Sleep Process.” 2014. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/1356.

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

MLA Handbook (7^th Edition):

Maguire, Sarah. “The "Ins and Outs" of Sleep: How Internal Metabolic and External Environmental Signals Affect the Sleep Process.” 2014. Web. 17 Oct 2019.

Vancouver:

Maguire S. The "Ins and Outs" of Sleep: How Internal Metabolic and External Environmental Signals Affect the Sleep Process. [Internet] [Thesis]. University of Pennsylvania; 2014. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/1356.

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

Council of Science Editors:

Maguire S. The "Ins and Outs" of Sleep: How Internal Metabolic and External Environmental Signals Affect the Sleep Process. [Thesis]. University of Pennsylvania; 2014. Available from: https://repository.upenn.edu/edissertations/1356

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

University of Pennsylvania

28. Rodriguez, Jason Christopher. Distinct Circuit States Enable State-dependent Flexibility in a Rhythm Generating Network.

Degree: 2014, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1422

► My thesis aimed to elucidate general organizing principles underlying the modulation of neural circuits. These circuits are flexible constructs that, when modulated, can occupy many… (more)

▼ My thesis aimed to elucidate general organizing principles underlying the modulation of neural circuits. These circuits are flexible constructs that, when modulated, can occupy many distinct states and produce different output patterns. Distinct circuit states can also produce the same output pattern in some cases. However, understanding the mechanisms and consequences of this latter phenomenon is impossible to achieve without the capability to observe and manipulate the cellular and synaptic properties of all circuit neurons. This work takes advantage of our detailed, cellular-level access to the central pattern generator (CPG) circuits found in the decapod crustacean stomatogastric nervous system, a specialized extension of the CNS dedicated to internal feeding-related behaviors. As CPGs are rhythmically active networks, much of this work focuses on the ability of such circuits to produce rhythmic output patterns (i.e. rhythm generation). Using this system, I found that distinct circuit states (configured by MCN1 projection neuron stimulation and CabPK peptide application) can enable comparable rhythm generation by recruiting distinct ionic conductances with overlapping functional roles (i.e. IMI and ITrans-LTS), each being regulated by synaptic inhibition to produce phasic excitatory drive to a pivotal circuit neuron (LG). In one case (MCN1 stimulation), the conductance is activated by a modulatory peptide transmitter whose release is regulated by presynaptic feedback inhibition. In the other case (CabPK application), the conductance has a slow inactivation property that is removed by hyperpolarization caused by synaptic inhibition. I also describe the consequences of having different circuit states that produce identical outputs by assaying their responses to the same, well-defined modulatory inputs - peptide (CCAP) hormone modulation and sensory feedback (GPR neuron). I found that hormonal modulation produced opposite effects on these two circuits states even though the cellular-level hormonal action is likely the same in both states. In contrast, I found these circuits were similarly sensitive to sensory feedback, despite this feedback acting via different synapses under each condition. My work thereby provides the first mechanistic understanding of input-pathway specific rhythm generators that produce convergent output patterns and the flexibility enabled by these circuit states when responding to additional modulatory inputs.

Subjects/Keywords: Neuroscience and Neurobiology

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

APA (6^th Edition):

Rodriguez, J. C. (2014). Distinct Circuit States Enable State-dependent Flexibility in a Rhythm Generating Network. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1422

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):

Rodriguez, Jason Christopher. “Distinct Circuit States Enable State-dependent Flexibility in a Rhythm Generating Network.” 2014. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/1422.

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

MLA Handbook (7^th Edition):

Rodriguez, Jason Christopher. “Distinct Circuit States Enable State-dependent Flexibility in a Rhythm Generating Network.” 2014. Web. 17 Oct 2019.

Vancouver:

Rodriguez JC. Distinct Circuit States Enable State-dependent Flexibility in a Rhythm Generating Network. [Internet] [Thesis]. University of Pennsylvania; 2014. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/1422.

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

Council of Science Editors:

Rodriguez JC. Distinct Circuit States Enable State-dependent Flexibility in a Rhythm Generating Network. [Thesis]. University of Pennsylvania; 2014. Available from: https://repository.upenn.edu/edissertations/1422

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

University of Pennsylvania

29. Neuhaus-Follini, Alexandra. The Intracellular Domain of the Frazzled/Dcc Receptor is a Transcription Factor Required for Commissural Axon Guidance.

Degree: 2015, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1102

► During embryonic development, conserved families of attractive and repulsive cues steer axons by signaling through receptors that are expressed on axonal growth cones. In the… (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):

Neuhaus-Follini, A. (2015). The Intracellular Domain of the Frazzled/Dcc Receptor is a Transcription Factor Required for Commissural Axon Guidance. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1102

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):

Neuhaus-Follini, Alexandra. “The Intracellular Domain of the Frazzled/Dcc Receptor is a Transcription Factor Required for Commissural Axon Guidance.” 2015. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/1102.

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

MLA Handbook (7^th Edition):

Neuhaus-Follini, Alexandra. “The Intracellular Domain of the Frazzled/Dcc Receptor is a Transcription Factor Required for Commissural Axon Guidance.” 2015. Web. 17 Oct 2019.

Vancouver:

Neuhaus-Follini A. The Intracellular Domain of the Frazzled/Dcc Receptor is a Transcription Factor Required for Commissural Axon Guidance. [Internet] [Thesis]. University of Pennsylvania; 2015. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/1102.

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

Council of Science Editors:

Neuhaus-Follini A. The Intracellular Domain of the Frazzled/Dcc Receptor is a Transcription Factor Required for Commissural Axon Guidance. [Thesis]. University of Pennsylvania; 2015. Available from: https://repository.upenn.edu/edissertations/1102

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

University of Pennsylvania

30. Shilling, Dustin J. Examinations into the Calcium Hypothesis of Alzheimer's Disease.

Degree: 2013, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/697

► Alzheimer's disease (AD) is devastating to the patient, their family and friends, and represents a significant fiscal burden to our society. Currently available therapeutics provide… (more)

▼ Alzheimer's disease (AD) is devastating to the patient, their family and friends, and represents a significant fiscal burden to our society. Currently available therapeutics provide only mild symptomatic relief and do not alter the course of the disease. Developing the next generation of disease modifying therapies requires an understanding of the early cellular changes responsible for AD. A hindrance to progress is the fact that most patients develop AD sporadically. However, mutations in the presenilin (PS) homologs cause dominantly inherited, early-onset AD. These mutations provide an important tool for understanding the cellular changes that cause AD. One consequence of PS mutations is exaggerated intracellular Ca2+ ([Ca2+]i) signaling. However, the mechanisms underlying this phenomenon remain controversial and its role in AD pathogenesis is unknown. Presented here are data indicating that exaggerated [Ca2+]i signaling is dependent upon the inositol 1,4,5-trisphosphate receptor (InsP3R) and contributes to AD pathogenesis in vivo. We began our studies by testing multiple proposed mechanisms for exaggerated [Ca2+]i signaling. To do this we employed multiple Ca2+ imaging protocols and Ca2+ indicators to directly measure ER Ca2+ dynamics in several cell systems. We found that decreasing InsP3R protein level rescues exaggerated [Ca2+]i signaling in primary cortical neurons and hippocampal slices from mutant PS1 expressing mice. We then determined the contribution of exaggerated [Ca2+]i signaling to AD pathogenesis. Using a combination of genetic, biochemical, electrophysiological and behavioral techniques, we found that rescue of exaggerated [Ca2+]i signaling dramatically attenuates mild cognitive impairment and AD phenotypes in AD mouse models. Reduction of InsP3R1 protein level in PS1M146V-KIN mice rescued enhanced hippocampal ryanodine receptor protein level, enhanced hippocampal synaptic potentiation, and constitutive activation of the CaMKIV-CREB transcriptional pathway. In 3xTg mice, reduced InsP3R1 protein level attenuated Aβ and phospho-tau accumulation and hippocampal electrophysiology and memory impairments. Together, these results reveal that mutant PS-associated exaggerated [Ca2+]i signaling is InsP3R1-dependent, a proximal event, and contributes to the development of AD in vivo. These findings advance our understanding of the pathological role of exaggerated [Ca2+]i signaling in AD and identify several novel targets for the development of disease modifying therapeutics.

Subjects/Keywords: Neuroscience and Neurobiology

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

APA (6^th Edition):

Shilling, D. J. (2013). Examinations into the Calcium Hypothesis of Alzheimer's Disease. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/697

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):

Shilling, Dustin J. “Examinations into the Calcium Hypothesis of Alzheimer's Disease.” 2013. Thesis, University of Pennsylvania. Accessed October 17, 2019. https://repository.upenn.edu/edissertations/697.

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

MLA Handbook (7^th Edition):

Shilling, Dustin J. “Examinations into the Calcium Hypothesis of Alzheimer's Disease.” 2013. Web. 17 Oct 2019.

Vancouver:

Shilling DJ. Examinations into the Calcium Hypothesis of Alzheimer's Disease. [Internet] [Thesis]. University of Pennsylvania; 2013. [cited 2019 Oct 17]. Available from: https://repository.upenn.edu/edissertations/697.

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

Council of Science Editors:

Shilling DJ. Examinations into the Calcium Hypothesis of Alzheimer's Disease. [Thesis]. University of Pennsylvania; 2013. Available from: https://repository.upenn.edu/edissertations/697

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

Open Access Theses and Dissertations