subject:(Astrocytes physiology)

Michigan State University

1. Ramsell, Katrina Dee. Biochemical mechanisms mediating morphological plasticity of astrolgial cells in culture.

Degree: PhD, Department of Pharmacology and Toxicology, 1997, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:27084

Subjects/Keywords: Neurophysiology; Brain – Physiology; Astrocytes

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APA (6^th Edition):

Ramsell, K. D. (1997). Biochemical mechanisms mediating morphological plasticity of astrolgial cells in culture. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:27084

Chicago Manual of Style (16^th Edition):

Ramsell, Katrina Dee. “Biochemical mechanisms mediating morphological plasticity of astrolgial cells in culture.” 1997. Doctoral Dissertation, Michigan State University. Accessed March 06, 2021. http://etd.lib.msu.edu/islandora/object/etd:27084.

MLA Handbook (7^th Edition):

Ramsell, Katrina Dee. “Biochemical mechanisms mediating morphological plasticity of astrolgial cells in culture.” 1997. Web. 06 Mar 2021.

Vancouver:

Ramsell KD. Biochemical mechanisms mediating morphological plasticity of astrolgial cells in culture. [Internet] [Doctoral dissertation]. Michigan State University; 1997. [cited 2021 Mar 06]. Available from: http://etd.lib.msu.edu/islandora/object/etd:27084.

Council of Science Editors:

Ramsell KD. Biochemical mechanisms mediating morphological plasticity of astrolgial cells in culture. [Doctoral Dissertation]. Michigan State University; 1997. Available from: http://etd.lib.msu.edu/islandora/object/etd:27084

University of Hong Kong

2. Ho, Chung-yin, Maggie. The functional role of endothelin-1 in astrocytes by making use of endothelin-1 knockout mice.

Degree: 2000, University of Hong Kong

URL: http://hdl.handle.net/10722/34005

Subjects/Keywords: Endothelins - Receptors.; Astrocytes.; Mice - Physiology.

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APA (6^th Edition):

Ho, Chung-yin, M. (2000). The functional role of endothelin-1 in astrocytes by making use of endothelin-1 knockout mice. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/34005

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):

Ho, Chung-yin, Maggie. “The functional role of endothelin-1 in astrocytes by making use of endothelin-1 knockout mice.” 2000. Thesis, University of Hong Kong. Accessed March 06, 2021. http://hdl.handle.net/10722/34005.

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

MLA Handbook (7^th Edition):

Ho, Chung-yin, Maggie. “The functional role of endothelin-1 in astrocytes by making use of endothelin-1 knockout mice.” 2000. Web. 06 Mar 2021.

Vancouver:

Ho, Chung-yin M. The functional role of endothelin-1 in astrocytes by making use of endothelin-1 knockout mice. [Internet] [Thesis]. University of Hong Kong; 2000. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/10722/34005.

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

Council of Science Editors:

Ho, Chung-yin M. The functional role of endothelin-1 in astrocytes by making use of endothelin-1 knockout mice. [Thesis]. University of Hong Kong; 2000. Available from: http://hdl.handle.net/10722/34005

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

Rutgers University

3. Huang, Yangyang, 1978-. Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes.

Degree: Biology, 2010, Rutgers University

URL: http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052961

Subjects/Keywords: Interleukin-1; Neurons – Physiology; Astrocytes

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APA (6^th Edition):

Huang, Yangyang, 1. (2010). Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes. (Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052961

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):

Huang, Yangyang, 1978-. “Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes.” 2010. Thesis, Rutgers University. Accessed March 06, 2021. http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052961.

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

MLA Handbook (7^th Edition):

Huang, Yangyang, 1978-. “Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes.” 2010. Web. 06 Mar 2021.

Vancouver:

Huang, Yangyang 1. Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes. [Internet] [Thesis]. Rutgers University; 2010. [cited 2021 Mar 06]. Available from: http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052961.

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

Council of Science Editors:

Huang, Yangyang 1. Interleukin-1 mediated cell-type specific signaling in hippocampal neurons and astrocytes. [Thesis]. Rutgers University; 2010. Available from: http://hdl.rutgers.edu/1782.2/rucore10002600001.ETD.000052961

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

4. Bellot-Saez, Alba. Astrocytic modulation of neuronal network oscillations.

Degree: 2019, Western Sydney University

URL: http://hdl.handle.net/1959.7/uws:54319

► The synchronization of the neuron’s membrane potential results in the emergence of neuronal oscillations at multiple frequencies that serve distinct physiological functions (e.g. facilitation of… (more)

▼ The synchronization of the neuron’s membrane potential results in the emergence of neuronal oscillations at multiple frequencies that serve distinct physiological functions (e.g. facilitation of synaptic plasticity) and correlate with different behavioural states (e.g. sleep, wakefulness, attention). It has been postulated that at least ten distinct mechanisms are required to cover the large frequency range of neuronal oscillations in the cortex, including variations in the concentration of extracellular neurotransmitters and ions, as well as changes in cellular excitability. However, the mechanism that gears the transition between different oscillatory frequencies is still unknown. Over the past decade, astrocytes have been the focus of much research, mainly due to (1) their close association with synapses forming what is known today as the “tripartite synapse”, which allows them to bidirectionally interact with neurons and modulate synaptic transmission; (2) their syncytium-like activity, as they are electrically coupled via gap junctions and actively communicate through Ca2+ waves; and (3) their ability to regulate neuronal excitability via glutamate uptake and tight control of the extracellular K+ levels via a process termed K+ clearance. In this thesis we hypothesized that astrocytes, in addition to their role as modulators of neuronal excitability, also act as “network managers” that can modulate the overall network oscillatory activity within their spatial domain. To do so, it is proposed that astrocytes fine-tune their K+ clearance capabilities to affect neuronal intrinsic excitability properties and synchronization with other neurons, thus mediating the transitions between neuronal network oscillations at different frequencies. To validate or reject this hypothesis I have investigated the potential role of astrocytes in modulating cortical oscillations at both cellular and network levels, aiming at answering three main research questions: a) what is the impact of alterations in astrocytic K+ clearance mechanisms on cortical networks oscillatory dynamics? b) what specific neuronal properties underlying the generation of neuronal oscillations are affected as a result of impairments in the astrocytic K+ clearance process? and c) what are the bidirectional mechanisms between neurons and astrocytes (i.e. neuromodulators) that specifically affect the K+ clearance process to modulate the network activity output? In the first experimental chapter I used electrophysiological recordings and pharmacological manipulations to dissect the contribution of the different astrocytic K+ clearance mechanisms to the modulation of neuronal network oscillations at multiple frequencies. A key finding was that alterations in membrane properties of layer V pyramidal neurons strongly correlated with the network behaviour following impairments in astrocytic K+ clearance capabilities, depicted as enhanced excitability underlying the amplification of high-frequency oscillations, especially within the beta and gamma range. The second… Advisors/Committee Members: Western Sydney University. School of Medicine (Host institution).

Subjects/Keywords: astrocytes; central nervous system; diseases; neurons; physiology; neural transmission; Thesis (Ph.D.) – Western Sydney University, 2019

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APA (6^th Edition):

Bellot-Saez, A. (2019). Astrocytic modulation of neuronal network oscillations. (Thesis). Western Sydney University. Retrieved from http://hdl.handle.net/1959.7/uws:54319

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):

Bellot-Saez, Alba. “Astrocytic modulation of neuronal network oscillations.” 2019. Thesis, Western Sydney University. Accessed March 06, 2021. http://hdl.handle.net/1959.7/uws:54319.

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

MLA Handbook (7^th Edition):

Bellot-Saez, Alba. “Astrocytic modulation of neuronal network oscillations.” 2019. Web. 06 Mar 2021.

Vancouver:

Bellot-Saez A. Astrocytic modulation of neuronal network oscillations. [Internet] [Thesis]. Western Sydney University; 2019. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/1959.7/uws:54319.

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

Council of Science Editors:

Bellot-Saez A. Astrocytic modulation of neuronal network oscillations. [Thesis]. Western Sydney University; 2019. Available from: http://hdl.handle.net/1959.7/uws:54319

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

5. Dzubay, Jeffrey A. Determinants of the time course of excitatory synaptic events in the CNS.

Degree: PhD, 1999, Oregon Health Sciences University

URL: doi:10.6083/M4H41PN1 ; http://digitalcommons.ohsu.edu/etd/2527

Subjects/Keywords: Synaptic Transmission; Receptors, Glutamate; Glutamic Acid – physiology; Neurons – physiology; Astrocytes – physiology

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

APA (6^th Edition):

Dzubay, J. A. (1999). Determinants of the time course of excitatory synaptic events in the CNS. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4H41PN1 ; http://digitalcommons.ohsu.edu/etd/2527

Chicago Manual of Style (16^th Edition):

Dzubay, Jeffrey A. “Determinants of the time course of excitatory synaptic events in the CNS.” 1999. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 06, 2021. doi:10.6083/M4H41PN1 ; http://digitalcommons.ohsu.edu/etd/2527.

MLA Handbook (7^th Edition):

Dzubay, Jeffrey A. “Determinants of the time course of excitatory synaptic events in the CNS.” 1999. Web. 06 Mar 2021.

Vancouver:

Dzubay JA. Determinants of the time course of excitatory synaptic events in the CNS. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1999. [cited 2021 Mar 06]. Available from: doi:10.6083/M4H41PN1 ; http://digitalcommons.ohsu.edu/etd/2527.

Council of Science Editors:

Dzubay JA. Determinants of the time course of excitatory synaptic events in the CNS. [Doctoral Dissertation]. Oregon Health Sciences University; 1999. Available from: doi:10.6083/M4H41PN1 ; http://digitalcommons.ohsu.edu/etd/2527

6. Ma, Ying Jun. Transforming growth factor alpha (TGFÎ±) of glial origin is a hypothalamic regulator of mammalian sexual development.

Degree: PhD, 1993, Oregon Health Sciences University

URL: doi:10.6083/M40G3H8K ; http://digitalcommons.ohsu.edu/etd/1695

Subjects/Keywords: Transforming Growth Factor alpha; Sexual Maturation; Astrocytes – physiology

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APA (6^th Edition):

Ma, Y. J. (1993). Transforming growth factor alpha (TGFÎ±) of glial origin is a hypothalamic regulator of mammalian sexual development. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M40G3H8K ; http://digitalcommons.ohsu.edu/etd/1695

Chicago Manual of Style (16^th Edition):

Ma, Ying Jun. “Transforming growth factor alpha (TGFÎ±) of glial origin is a hypothalamic regulator of mammalian sexual development.” 1993. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 06, 2021. doi:10.6083/M40G3H8K ; http://digitalcommons.ohsu.edu/etd/1695.

MLA Handbook (7^th Edition):

Ma, Ying Jun. “Transforming growth factor alpha (TGFÎ±) of glial origin is a hypothalamic regulator of mammalian sexual development.” 1993. Web. 06 Mar 2021.

Vancouver:

Ma YJ. Transforming growth factor alpha (TGFÎ±) of glial origin is a hypothalamic regulator of mammalian sexual development. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1993. [cited 2021 Mar 06]. Available from: doi:10.6083/M40G3H8K ; http://digitalcommons.ohsu.edu/etd/1695.

Council of Science Editors:

Ma YJ. Transforming growth factor alpha (TGFÎ±) of glial origin is a hypothalamic regulator of mammalian sexual development. [Doctoral Dissertation]. Oregon Health Sciences University; 1993. Available from: doi:10.6083/M40G3H8K ; http://digitalcommons.ohsu.edu/etd/1695

University of Oxford

7. Raimondo, Joseph Valentino. Intracellular chloride and hydrogen ion dynamics in the nervous system.

Degree: PhD, 2012, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:0b69b409-46e5-41ac-88c4-f1cfaf08ad24 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588398

► Synaptic transmission in the nervous system involves the activation of receptor proteins that permit rapid transmembrane fluxes of ions. Ionic gradients across the membrane determine… (more)

▼ Synaptic transmission in the nervous system involves the activation of receptor proteins that permit rapid transmembrane fluxes of ions. Ionic gradients across the membrane determine the direction and driving force for the flow of ions and are therefore crucial in setting the properties of synaptic transmission. These ionic gradients are established by a variety of mechanisms, including pump and transporter proteins. However, the gradients can be affected by periods of neural activity, which in turn, are predicted to influence the properties of ongoing synaptic transmission. In this thesis I have examined the concentration gradients of two ions that play a fundamental role in synaptic transmission: chloride ions (Cl-) and protons (H+). Type A γ-Aminobutyric acid receptors (GABAARs) are primarily permeable to Cl- and mediate the majority of fast post-synaptic inhibition in the brain. The transmembrane concentration gradient for Cl- is therefore a critical parameter in governing the strength of synaptic inhibition. In the first part of the Thesis I use a combination of experimental and theoretical approaches to demonstrate that influxes of Cl- via activated GABAARs can overwhelm a neurons ability to maintain a stable Cl- concentration gradient. The consequence is that subsequent activation of GABAARs results in weaker inhibition or even excitation, which alters how the neuron integrates synaptic inputs. This process is shown to be dependent upon the level of activity of the GABAAR, the post-synaptic cells membrane potential and the cellular compartment into which the Cl- flows. These principles were extended to demonstrate that popular optogenetic strategies for silencing neural activity have different effects upon GABAAR transmission. A light-activated Cl- pump was shown to cause substantial accumulations in intracellular Cl, which meant that the strength of synaptic inhibition was significantly reduced following light offset. In the second part of the Thesis I use electrophysiological and fluorescence imaging techniques to demonstrate that the activation of GABAARs during epileptiform activity results in pronounced changes to the transmembrane Cl- gradient. Indeed, these changes convert synaptic inhibition into synaptic excitation during the course of a seizure event. As part of this work I characterise a novel, genetically-encoded reporter for measuring intracellular Cl- dynamics in different cell types and subcellular compartments. A significant advantage of this reporter is that it permits the simultaneous quantification of H+ fluxes, which are also shown to change in an activity-dependent manner and which have been a confounding factor for previous Cl- reporters. In the third and final part of the Thesis I use genetically-encoded reporters to investigate activity-dependent changes in intracellular H+ concentration. I demonstrate that markedly different pH changes occur in neurons and astrocytes during epileptiform activity. Whereas neurons become acidic, astrocytes become alkaline and the dynamics of these pH…

Subjects/Keywords: 612.8; Biosensors; Biology (medical sciences); Medical Sciences; Physiology and anatomy; epilepsy; neuroscience; chloride; pH; astrocytes; neurons

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APA (6^th Edition):

Raimondo, J. V. (2012). Intracellular chloride and hydrogen ion dynamics in the nervous system. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:0b69b409-46e5-41ac-88c4-f1cfaf08ad24 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588398

Chicago Manual of Style (16^th Edition):

Raimondo, Joseph Valentino. “Intracellular chloride and hydrogen ion dynamics in the nervous system.” 2012. Doctoral Dissertation, University of Oxford. Accessed March 06, 2021. http://ora.ox.ac.uk/objects/uuid:0b69b409-46e5-41ac-88c4-f1cfaf08ad24 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588398.

MLA Handbook (7^th Edition):

Raimondo, Joseph Valentino. “Intracellular chloride and hydrogen ion dynamics in the nervous system.” 2012. Web. 06 Mar 2021.

Vancouver:

Raimondo JV. Intracellular chloride and hydrogen ion dynamics in the nervous system. [Internet] [Doctoral dissertation]. University of Oxford; 2012. [cited 2021 Mar 06]. Available from: http://ora.ox.ac.uk/objects/uuid:0b69b409-46e5-41ac-88c4-f1cfaf08ad24 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588398.

Council of Science Editors:

Raimondo JV. Intracellular chloride and hydrogen ion dynamics in the nervous system. [Doctoral Dissertation]. University of Oxford; 2012. Available from: http://ora.ox.ac.uk/objects/uuid:0b69b409-46e5-41ac-88c4-f1cfaf08ad24 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588398

Michigan State University

8. Mohr, Margaret Ann. Neuro- and gliogenesis in the pubertal rat brain : implications for female reproduction.

Degree: 2015, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:3480

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"The goal of the experiments conducted in this dissertation was to test the hypothesis that cells added to the AVPV [anteroventral periventricular nucleus] during puberty… (more)

Subjects/Keywords: Developmental neurobiology; Neuroendocrinology; Rats – Reproduction – Endocrine aspects; Veterinary neurology; Astrocytes; Luteinizing hormone; Rats – Physiology; Neurosciences; Endocrinology

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APA (6^th Edition):

Mohr, M. A. (2015). Neuro- and gliogenesis in the pubertal rat brain : implications for female reproduction. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:3480

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):

Mohr, Margaret Ann. “Neuro- and gliogenesis in the pubertal rat brain : implications for female reproduction.” 2015. Thesis, Michigan State University. Accessed March 06, 2021. http://etd.lib.msu.edu/islandora/object/etd:3480.

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

MLA Handbook (7^th Edition):

Mohr, Margaret Ann. “Neuro- and gliogenesis in the pubertal rat brain : implications for female reproduction.” 2015. Web. 06 Mar 2021.

Vancouver:

Mohr MA. Neuro- and gliogenesis in the pubertal rat brain : implications for female reproduction. [Internet] [Thesis]. Michigan State University; 2015. [cited 2021 Mar 06]. Available from: http://etd.lib.msu.edu/islandora/object/etd:3480.

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

Council of Science Editors:

Mohr MA. Neuro- and gliogenesis in the pubertal rat brain : implications for female reproduction. [Thesis]. Michigan State University; 2015. Available from: http://etd.lib.msu.edu/islandora/object/etd:3480

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

9. Reyes, Reno Cervo. The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes.

Degree: PhD, 2009, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,688

►

Astrocytes, a type of glial cell in the central nervous system, are recognized for their support roles to neurons. They supply neurons with metabolites, maintain… (more)

▼

Astrocytes, a type of glial cell in the central nervous system, are recognized for their support roles to neurons. They supply neurons with metabolites, maintain ion homeostasis and clear the synaptic space of neurotransmitters. However, it has been found that some astrocytes have receptors for neurotransmitter and neuroligands, exhibit Ca2+ excitability when stimulated via these receptors, and secrete gliotransmitters as an output of this Ca2+ excitability. In the Ca2+-dependent release of glutamate, it has been shown that the endoplasmic reticulum is the predominant source and the extracellular space is the auxiliary source of free Ca2+ necessary for triggering exocytosis. Because astrocytes possess mitochondria and plasma membrane Ca2+ transport systems that play roles in Ca2+ signaling in other cell types including neurons, I hypothesized that these elements also regulate Ca2+ signaling in astrocytes, and can modulate glutamate release. Employing cultured astroctyes from the visual cortex of newborn rats, I measured changes in cytosolic Ca2+ in stimulated astrocytes, and in parallel experiments measured glutamate release through a glutamate dehydrogenase assay. I took a pharmacological approach to manipulate the Ca2+ handling of mitochondria and the plasma membrane Ca2+ transport systems. I showed that regulation of Ca2+ signaling by mitochondria and the plasma membrane Ca2+ transport systems correlates with modulation of glutamate release where an increase in cytosolic Ca2+ resulted in increase glutamate release. These studies expand what is known about Ca2+ signaling and exocytotic transmitter release in astrocytes. These studies may have medical relevance since the importance of Ca2+ signaling in astrocytes has been implicated in models of various neurological diseases.

1 online resource (x, 141 p. : ill., digital, PDF file)

Neurobiology;

Joint Health Sciences;

astrocytes Ca2+ mitochondria plasma membrane exocytosis glutamate

UNRESTRICTED

Advisors/Committee Members: Parpura, Vladimir, Lesort, Mathieu Jean , McMahon-Wakefield, Lori L. , Sontheimer, Harald W. , Wadiche, Jacques.

Subjects/Keywords: Astrocytes – metabolism<; br>; Astrocytes – ultrastructure<; br>; Calcium – metabolism<; br>; Exocytosis – physiology<; br>; Glutamic Acid – metabolism<; br>; Mitochondria – physiology<; br>; Visual Cortex – cytology

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

APA (6^th Edition):

Reyes, R. C. (2009). The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,688

Chicago Manual of Style (16^th Edition):

Reyes, Reno Cervo. “The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,688.

MLA Handbook (7^th Edition):

Reyes, Reno Cervo. “The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes.” 2009. Web. 06 Mar 2021.

Vancouver:

Reyes RC. The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,688.

Council of Science Editors:

Reyes RC. The role of mitochondria and plasma membrane CA²⁺ transport systems in CA²⁺-dependent glutamate release from rat cortical astrocytes. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,688

Loma Linda University

10. Stout, Charles Emmet. Mechanisms of Calcium Wave Initiation and Propagation in Astrocytes.

Degree: PhD, Physiology, 2002, Loma Linda University

URL: https://scholarsrepository.llu.edu/etd/925

► Glial cells display propagated waves of cytoplasmic calcium (Ca²⁺) mobilization that spread outward from an initiating cell to involve hundreds to thousands of surrounding… (more)

▼ Glial cells display propagated waves of cytoplasmic calcium (Ca²⁺) mobilization that spread outward from an initiating cell to involve hundreds to thousands of surrounding cells. This intercellular communication system is thought to initiate and coordinate Ca²⁺ dependent processes associated with vascular control, gut motility, uterine contraction, and synaptic plasticity. Not surprisingly, aberrant Ca signaling is thought to play a featured role in the pathophysiologies associated with dysfunction of these processes. This suggests that elucidation of the mechanism of Ca²⁺ waves will lead to rational therapeutic modalities for a variety of clinically significant entities. Early studies revealed that Ca²⁺ waves in glia require the expression and function of the gap junction protein connexin43 (Cx43), the function of phospholipase C (PEC) and the mobilization of Ca²⁺ from inositol-1,4,5-trisphosphate (IP3) dependent stores. This lead to the hypothesis that Ca waves are mediated by mobilization of IP3 in the stimulated cell that then diffuses to surrounding cells through gap junctions composed of Cx43 where it initiates Ca²⁺ mobilization from IP3 dependent stores. Subsequently, this hypothesis was confounded by the discovery that Ca²⁺waves are mediated by ATP diffusion in the extracellular space. This confusion arose because Cx43 channels are most studied in the gap junction configuration and no role could easily be ascribed to an intercellular channel in an extracellular paracrine signaling system. Cx43 channels also exist, however, in a hemichannel configuration that gates between the cytoplasm and the extracellular space. The main discovery of this dissertation is that it is the hemichannel configuration that is required for Ca²⁺ waves. Specifically, Cx43 hemichannels mediate the release of ATP into the extracellular space to initiate and sustain glial Ca²⁺ waves. Further, it is demonstrated that diacylglycerol mobilization is associated with hemichannel activation 9-f- indicating a new role of PLC activity in Ca²⁺ wave propagation. Finally, modulation of this ATP release pathway by several agents, including those with clinical significance, is 9-4- demonstrated to be directly correlated with modulation of Ca wave propagation suggesting that modulation of ATP release represents a viable target for rational therapeutic treatment of disorders that arise from aberrant Ca²⁺ signaling. Advisors/Committee Members: J. Mailen Kootsey, Andrew Charles, John Buchhlolz, George Maeda, William J. Pearce.

Subjects/Keywords: Cellular and Molecular Physiology; Astrocytes – physiology; Calcium Channels – metabolism; Calcium Signaling.

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APA (6^th Edition):

Stout, C. E. (2002). Mechanisms of Calcium Wave Initiation and Propagation in Astrocytes. (Doctoral Dissertation). Loma Linda University. Retrieved from https://scholarsrepository.llu.edu/etd/925

Chicago Manual of Style (16^th Edition):

Stout, Charles Emmet. “Mechanisms of Calcium Wave Initiation and Propagation in Astrocytes.” 2002. Doctoral Dissertation, Loma Linda University. Accessed March 06, 2021. https://scholarsrepository.llu.edu/etd/925.

MLA Handbook (7^th Edition):

Stout, Charles Emmet. “Mechanisms of Calcium Wave Initiation and Propagation in Astrocytes.” 2002. Web. 06 Mar 2021.

Vancouver:

Stout CE. Mechanisms of Calcium Wave Initiation and Propagation in Astrocytes. [Internet] [Doctoral dissertation]. Loma Linda University; 2002. [cited 2021 Mar 06]. Available from: https://scholarsrepository.llu.edu/etd/925.

Council of Science Editors:

Stout CE. Mechanisms of Calcium Wave Initiation and Propagation in Astrocytes. [Doctoral Dissertation]. Loma Linda University; 2002. Available from: https://scholarsrepository.llu.edu/etd/925

11. Harrison, John M. (John Martin). Receptor occupancy and time course of excitatory synaptic events in the CNS.

Degree: PhD, 2005, Oregon Health Sciences University

URL: doi:10.6083/M4B856DF ; http://digitalcommons.ohsu.edu/etd/2954

Subjects/Keywords: Amino Acid Transport System X-AG – physiology; Purkinje Cells – physiology; Pyramidal Cells – physiology; Glutamic Acid – physiology; Astrocytes – physiology

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

APA (6^th Edition):

Harrison, J. M. (. M. (2005). Receptor occupancy and time course of excitatory synaptic events in the CNS. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4B856DF ; http://digitalcommons.ohsu.edu/etd/2954

Chicago Manual of Style (16^th Edition):

Harrison, John M (John Martin). “Receptor occupancy and time course of excitatory synaptic events in the CNS.” 2005. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 06, 2021. doi:10.6083/M4B856DF ; http://digitalcommons.ohsu.edu/etd/2954.

MLA Handbook (7^th Edition):

Harrison, John M (John Martin). “Receptor occupancy and time course of excitatory synaptic events in the CNS.” 2005. Web. 06 Mar 2021.

Vancouver:

Harrison JM(M. Receptor occupancy and time course of excitatory synaptic events in the CNS. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2005. [cited 2021 Mar 06]. Available from: doi:10.6083/M4B856DF ; http://digitalcommons.ohsu.edu/etd/2954.

Council of Science Editors:

Harrison JM(M. Receptor occupancy and time course of excitatory synaptic events in the CNS. [Doctoral Dissertation]. Oregon Health Sciences University; 2005. Available from: doi:10.6083/M4B856DF ; http://digitalcommons.ohsu.edu/etd/2954

Texas Medical Center

12. Howe, Matthew D. The Role of Perivascular FIbrosis in Post-Stroke Glymphatic Impairment and Cerebral Amyloid Angiopathy.

Degree: PhD, 2018, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/875

► In healthy brain tissue, toxic amyloid-β (Aβ) proteins are transported by the pulsatile flow of cerebrospinal fluid (CSF) along perivascular drainage pathways. Ischemic stroke… (more)

Subjects/Keywords: Stroke; Fibronectin; Integrin; Amyloid; CAA; Glymphatic; CSF; TGF-beta; Astrocytes; Neurodegeneration; Biology; Cellular and Molecular Physiology; Medicine and Health Sciences; Molecular and Cellular Neuroscience; Pharmacology; Translational Medical Research

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

APA (6^th Edition):

Howe, M. D. (2018). The Role of Perivascular FIbrosis in Post-Stroke Glymphatic Impairment and Cerebral Amyloid Angiopathy. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/875

Chicago Manual of Style (16^th Edition):

Howe, Matthew D. “The Role of Perivascular FIbrosis in Post-Stroke Glymphatic Impairment and Cerebral Amyloid Angiopathy.” 2018. Doctoral Dissertation, Texas Medical Center. Accessed March 06, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/875.

MLA Handbook (7^th Edition):

Howe, Matthew D. “The Role of Perivascular FIbrosis in Post-Stroke Glymphatic Impairment and Cerebral Amyloid Angiopathy.” 2018. Web. 06 Mar 2021.

Vancouver:

Howe MD. The Role of Perivascular FIbrosis in Post-Stroke Glymphatic Impairment and Cerebral Amyloid Angiopathy. [Internet] [Doctoral dissertation]. Texas Medical Center; 2018. [cited 2021 Mar 06]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/875.

Council of Science Editors:

Howe MD. The Role of Perivascular FIbrosis in Post-Stroke Glymphatic Impairment and Cerebral Amyloid Angiopathy. [Doctoral Dissertation]. Texas Medical Center; 2018. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/875

University of Oxford

13. Al Dalahmah, Osama Ahmad Odeh. The molecular regulation of neural stem cell lineage progression in the postnatal subventricular zone by Galectin-3.

Degree: PhD, 2015, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:cb9020e1-931f-44cd-8409-7d2c58817d6e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682698

► Neurogenesis continues postnatally in two major neural stem cell (NSC) niches: The subventricular zone (SVZ) and dentate gurus of the hippocampus. SVZ NSCs self-renew and… (more)

▼ Neurogenesis continues postnatally in two major neural stem cell (NSC) niches: The subventricular zone (SVZ) and dentate gurus of the hippocampus. SVZ NSCs self-renew and produce transit amplifying progenitor cells that, in turn, divide and give rise to neuroblasts. These neuroblasts migrate to the olfactory bulbs, via the rostral migratory stream (RMS), where they terminally differentiate into mature neurons. The postnatal SVZ (pSVZ) is more gliogenic than its adult counterpart (aSVZ), contributing to robust postnatal astrocytogenesis and oligodendrogenesis in the surrounding brain parenchyma. Studies examining Galectin-3 (Gal-3) in the aSVZ showed it has functions in regulating neuroblast migration, microglial activation, oligodendrocytic differentiation, and angiogenesis. However, the role of Gal-3 in pSVZ lineage progression is unknown. This thesis aims to unravel the roles of Gal-3 in regulating pSVZ lineage progression, fate choices, and NSC activation. In doing so, the thesis tackles the molecular pathways possibly involved in mediating the effects of Gal-3. I found through co-immunoprecipitation that Gal-3 was bound to β-catenin and both proteins were co-expressed in the aSVZ. In addition, expression of Gal-3 and Wnt/β-catenin signalling were downregulated as SVZ cells progressed through the lineage and became migratory. I hypothesised that Gal-3 may regulate lineage progression through regulation of Wnt/β-catenin signalling. To explore this hypothesis, Gal-3 overexpression, knockdown or control plasmids were co-electroporated with a Wnt/β-catenin reporter into the SVZ of postnatal day two mice. I found lineage progression was not altered by Gal-3 overexpression. Surprisingly, contrary to evidence described in the cancer literature, Gal-3 overexpression reduced Wnt/β-catenin signalling. This was accompanied by an acute reduction in proliferation. Also, more cells expressed p27/Kip1 in the SVZ, and more cells migrated into the RMS, suggesting increased cell cycle exit. However, NSC proliferation and clonal neurosphere forming capacity were not altered by Gal-3 overexpression, indicating that NSC activation was not influenced by Gal-3. While olfactory neuronogenesis was not altered by Gal-3 overexpression, striatal astrocytogenesis was increased while oligodendrogenesis was dampened. Further experiments revealed phosphorylation of Smad proteins 1/5/8 was increased in vivo and in vitro after Gal-3 overexpression. These findings indicate that Gal-3 positively regulated BMP signalling in the SVZ, possibly contributing to Gal-3's pro-gliogenic effects. Taken together, this thesis supports a model whereby a subpopulation of Gal-3-responsive pSVZ cells reacted to Gal-3 overexpression by acutely exiting the cell cycle, and possibly through the same mechanisms, switched from oligodendrocytic to astrocytic fate. These cellular responses might have been brought about, at least partially, by acute suppression of Wnt/β-catenin and activation of BMP signalling. These novel findings emphasise…

Subjects/Keywords: 612.8; Biology; Physiology and anatomy; Transgenics; Anatomy; Neuroscience; Neurogenetics; Stem cells; Subventricular zone; Neural stem cells; Astrocytes; Oligodendrocytes; Galectin-3; Wnt/B-catenin; cell signalling

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

APA (6^th Edition):

Al Dalahmah, O. A. O. (2015). The molecular regulation of neural stem cell lineage progression in the postnatal subventricular zone by Galectin-3. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:cb9020e1-931f-44cd-8409-7d2c58817d6e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682698

Chicago Manual of Style (16^th Edition):

Al Dalahmah, Osama Ahmad Odeh. “The molecular regulation of neural stem cell lineage progression in the postnatal subventricular zone by Galectin-3.” 2015. Doctoral Dissertation, University of Oxford. Accessed March 06, 2021. http://ora.ox.ac.uk/objects/uuid:cb9020e1-931f-44cd-8409-7d2c58817d6e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682698.

MLA Handbook (7^th Edition):

Al Dalahmah, Osama Ahmad Odeh. “The molecular regulation of neural stem cell lineage progression in the postnatal subventricular zone by Galectin-3.” 2015. Web. 06 Mar 2021.

Vancouver:

Al Dalahmah OAO. The molecular regulation of neural stem cell lineage progression in the postnatal subventricular zone by Galectin-3. [Internet] [Doctoral dissertation]. University of Oxford; 2015. [cited 2021 Mar 06]. Available from: http://ora.ox.ac.uk/objects/uuid:cb9020e1-931f-44cd-8409-7d2c58817d6e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682698.

Council of Science Editors:

Al Dalahmah OAO. The molecular regulation of neural stem cell lineage progression in the postnatal subventricular zone by Galectin-3. [Doctoral Dissertation]. University of Oxford; 2015. Available from: http://ora.ox.ac.uk/objects/uuid:cb9020e1-931f-44cd-8409-7d2c58817d6e ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682698

14. Salameh, Ahlam Ibrahim. METABOLIC ACIDOSIS AND THE DIVERSE ROLES OF THE Cl/HCO₃ EXCHANGER (AE3) IN INTRACELLULAR pH HOMEOSTASIS.

Degree: PhD, Physiology and Biophysics, 2016, Case Western Reserve University School of Graduate Studies

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1473852052811835

► In this dissertation, I examine the effects of extracellular metabolic acidosis (MAc)—a decrease in extracellular pH (pH_o) caused by a decrease in [HCO₃^–]_o at fixed… (more)

Subjects/Keywords: Physiology; Nanoscience; Astrocytes; Cancer; Crosstalk; Dendritic Cells; Epilepsy; Hippocampus; Keratinocytes; Macrophages; Melanocytes; Mudullary raphe; Neurons; pH-regulation; Recovery Rate; Skeletal Muscles; Slc4

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

APA (6^th Edition):

Salameh, A. I. (2016). METABOLIC ACIDOSIS AND THE DIVERSE ROLES OF THE Cl/HCO₃ EXCHANGER (AE3) IN INTRACELLULAR pH HOMEOSTASIS. (Doctoral Dissertation). Case Western Reserve University School of Graduate Studies. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1473852052811835

Chicago Manual of Style (16^th Edition):

Salameh, Ahlam Ibrahim. “METABOLIC ACIDOSIS AND THE DIVERSE ROLES OF THE Cl/HCO₃ EXCHANGER (AE3) IN INTRACELLULAR pH HOMEOSTASIS.” 2016. Doctoral Dissertation, Case Western Reserve University School of Graduate Studies. Accessed March 06, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1473852052811835.

MLA Handbook (7^th Edition):

Salameh, Ahlam Ibrahim. “METABOLIC ACIDOSIS AND THE DIVERSE ROLES OF THE Cl/HCO₃ EXCHANGER (AE3) IN INTRACELLULAR pH HOMEOSTASIS.” 2016. Web. 06 Mar 2021.

Vancouver:

Salameh AI. METABOLIC ACIDOSIS AND THE DIVERSE ROLES OF THE Cl/HCO₃ EXCHANGER (AE3) IN INTRACELLULAR pH HOMEOSTASIS. [Internet] [Doctoral dissertation]. Case Western Reserve University School of Graduate Studies; 2016. [cited 2021 Mar 06]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1473852052811835.

Council of Science Editors:

Salameh AI. METABOLIC ACIDOSIS AND THE DIVERSE ROLES OF THE Cl/HCO₃ EXCHANGER (AE3) IN INTRACELLULAR pH HOMEOSTASIS. [Doctoral Dissertation]. Case Western Reserve University School of Graduate Studies; 2016. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1473852052811835

University of St. Andrews

15. Acton, David. Regulation of mammalian spinal locomotor networks by glial cells .

Degree: 2017, University of St. Andrews

URL: http://hdl.handle.net/10023/10133

► Networks of interneurons within the spinal cord coordinate the rhythmic activation of muscles during locomotion. These networks are subject to extensive neuromodulation, ensuring appropriate behavioural… (more)

▼ Networks of interneurons within the spinal cord coordinate the rhythmic activation of muscles during locomotion. These networks are subject to extensive neuromodulation, ensuring appropriate behavioural output. Astrocytes are proposed to detect neuronal activity via Gαq-linked G-protein coupled receptors and to secrete neuromodulators in response. However, there is currently a paucity of evidence that astrocytic information processing of this kind is important in behaviour. Here, it is shown that protease-activated receptor-1 (PAR1), a Gαq-linked receptor, is preferentially expressed by glia in the spinal cords of postnatal mice. During ongoing locomotor-related network activity in isolated spinal cords, PAR1 activation stimulates release of adenosine triphosphate (ATP), which is hydrolysed to adenosine extracellularly. Adenosine then activates A1 receptors to reduce the frequency of locomotor-related bursting recorded from ventral roots. This entails inhibition of D1 dopamine receptors, activation of which enhances burst frequency. The effect of A1 blockade scales with network activity, consistent with activity-dependent production of adenosine by glia. Astrocytes also regulate activity by controlling the availability of D-serine or glycine, both of which act as co-agonists of glutamate at N-methyl-D-aspartate receptors (NMDARs). The importance of NMDAR regulation for locomotor-related activity is demonstrated by blockade of NMDARs, which reduces burst frequency and amplitude. Bath-applied D-serine increases the frequency of locomotor-related bursting but not intense synchronous bursting produced by blockade of inhibitory transmission, implying activity-dependent regulation of co-agonist availability. Depletion of endogenous D-serine increases the frequency of locomotor-related but not synchronous bursting, indicating that D-serine is required at a subset of NMDARs expressed by inhibitory interneurons. Blockade of the astrocytic glycine transporter GlyT1 increases the frequency of locomotor-related activity, but application of glycine has no effect, indicating that GlyT1 regulates glycine at excitatory synapses. These results indicate that glia play an important role in regulating the output of spinal locomotor networks. Advisors/Committee Members: Miles, Gareth Brian (advisor).

Subjects/Keywords: Spinal cord physiology; Locomotion; Central pattern generator; CPG; Motor control; NMDA receptors; Glia; Glial cells; Astrocytes; Neural networks; Gliotransmission; PAR1; Dopamine; Co-agonist; D-serine; Glycine; GlyT1

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

APA (6^th Edition):

Acton, D. (2017). Regulation of mammalian spinal locomotor networks by glial cells . (Thesis). University of St. Andrews. Retrieved from http://hdl.handle.net/10023/10133

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):

Acton, David. “Regulation of mammalian spinal locomotor networks by glial cells .” 2017. Thesis, University of St. Andrews. Accessed March 06, 2021. http://hdl.handle.net/10023/10133.

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

MLA Handbook (7^th Edition):

Acton, David. “Regulation of mammalian spinal locomotor networks by glial cells .” 2017. Web. 06 Mar 2021.

Vancouver:

Acton D. Regulation of mammalian spinal locomotor networks by glial cells . [Internet] [Thesis]. University of St. Andrews; 2017. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/10023/10133.

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

Council of Science Editors:

Acton D. Regulation of mammalian spinal locomotor networks by glial cells . [Thesis]. University of St. Andrews; 2017. Available from: http://hdl.handle.net/10023/10133

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

16. Baker, Brandi J. Oncostatin M-induced gene expression and regulation in astrocytes and microglia.

Degree: PhD, 2009, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,560

►

Astrocytes and microglia are specialized glial cells of the Central Nervous System (CNS) that modulate neural activity and regulate immunological and inflammatory events. These cells… (more)

▼

Astrocytes and microglia are specialized glial cells of the Central Nervous System (CNS) that modulate neural activity and regulate immunological and inflammatory events. These cells perform their functions, in part, through the secretion of soluble mediators such as cytokines and chemokines. However, in response to the same neurological insult or inflammatory stimuli, the responses of these cells can vary greatly. This notion of differential responses was examined in our studies using Oncostatin M (OSM). OSM is a member of the IL-6 family of cytokines, which can be produced by microglia, astrocytes, neurons, and infiltrating leukocytes in the CNS, and is upregulated in a number of neuroinflammatory diseases. However, its effects within the CNS are not well understood. In astrocytes, OSM induces the expression of Suppressor Of Cytokine Signaling-3 (SOCS-3), a potent negative regulator of inflammatory cytokine signaling. However, OSM does not induce SOCS-3 expression in microglia. Similarly, OSM induces the production of the pro-inflammatory cytokine tumor necrosis factor-[Alpha] (TNF-[Alpha]) and inducible nitric oxide synthase (iNOS) from microglia, which are not expressed by astrocytes when exposed to OSM. The mechanisms of OSM-induced SOCS-3 and OSM-induced TNF-[Alpha] and iNOS expression were examined in astrocytes and microglia, respectively. In astrocytes, OSM utilizes the JAK/STAT and MAPK pathways to induce SOCS-3 expression. In microglia, OSM induces TNF-[Alpha] and iNOS expression via the NF-κB pathway, which also partially requires the intermediate production of TNF-[Alpha]. Interestingly, OSM does not activate the JAK/STAT pathway in microglia. Supernatants from OSM-treated microglia impair neuronal cell viability, which can be rescued by co-treating microglia with IL-27, a cytokine that inhibits OSM-mediated NF-κB activation and production of TNF-[Alpha] and NO. Therefore, OSM exposure of astrocytes and microglia leads to differential activation of signaling pathways and gene expression, underscoring the importance of cell-typespecific modulation in immunotherapies.

1 online resource (viii, 163 p. : ill., digital, PDF file)

Cell Biology;

Joint Health Sciences;

oncostatin M astrocytes SOCS microglia TNF-[Alpha] iNOS

UNRESTRICTED

Advisors/Committee Members: Benveniste, Etty (Tika) N., Brenner, Michael , Collawn, Jim , Frank, Stuart J. , Wakefield, Lori McMahon.

Subjects/Keywords: Astrocytes – physiology<; br>; Central Nervous System – immunology<; br>; Central Nervous System Diseases – immunology<; br>; Gene Expression Regulation – physiology<; br>; Microglia – physiology<; br>; Oncostatin M – physiology<; br>; Suppressor of Cytokine Signaling Proteins – biosynthesis<; br>; Suppressor of Cytokine Signaling Proteins – metabolism

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

APA (6^th Edition):

Baker, B. J. (2009). Oncostatin M-induced gene expression and regulation in astrocytes and microglia. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,560

Chicago Manual of Style (16^th Edition):

Baker, Brandi J. “Oncostatin M-induced gene expression and regulation in astrocytes and microglia.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,560.

MLA Handbook (7^th Edition):

Baker, Brandi J. “Oncostatin M-induced gene expression and regulation in astrocytes and microglia.” 2009. Web. 06 Mar 2021.

Vancouver:

Baker BJ. Oncostatin M-induced gene expression and regulation in astrocytes and microglia. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,560.

Council of Science Editors:

Baker BJ. Oncostatin M-induced gene expression and regulation in astrocytes and microglia. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,560

17. Yeo, Sujeong. Transcriptional Regulation Of Gfap.

Degree: 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1661

►

Glial fibrillary acidic protein (GFAP) is an astrocytic intermediate filament protein whose levels are increased in response to CNS injuries. Aim one of my thesis… (more)

▼

Glial fibrillary acidic protein (GFAP) is an astrocytic intermediate filament protein whose levels are increased in response to CNS injuries. Aim one of my thesis is to find the regulatory elements of the <italic>GFAP</italic> promoter responsible for its expression properties using a transgenic approach, since previous studies showed inconsistent results between <italic>in vitro</italic> and <italic>in vivo</italic> approaches. Two contiguous DNA segments previously implicated in transcriptional control of the <italic>GFAP</italic> gene, the B region (bp -1612 to -1489), and the C1.1 and C1.2 regions (bp -1488 to -1399), were analyzed. Block mutation of each of 4 contiguous sequences together spanning the B region decreased the level of promoter activity by at least 50%, indicating that each subregion contains the sites that cooperatively contribute to transcription. Several of the block mutations also altered the brain region pattern of expression, astrocyte specificity and/or the developmental time course. Effects on expression pattern and specificity had previously been observed for C1.1 and C1.2 block mutations. To identify the specific transcription factors involved, candidate binding sites were mutated in each of the 4 B block segments as well as in C1.1 and C1.2. Mutation of the AP-1 site unexpectedly had no effect, confirming that <italic>in vitro</italic> and <italic>in vivo</italic> regulation of <italic>GFAP</italic> transcription differ. Mutation of the SP1 site significantly reduced promoter activity, indicating that SP1 is a novel <italic>GFAP</italic> trancriptional activator. Mutations of either the NFI or NF-&kappaB site resulted in significant transgene expression in hippocampal neurons, suggesting that they act to suppress <italic>GFAP</italic> expression in neurons. My second aim was to find the epigenetic mechanisms associated with region specific expression of a transgene driven by a shortened <italic>GFAP</italic> promoter, gfaABD (bp -1757 to -1489 linked to -132 to +56). I found that histone methylation, but not DNA methylation, is correlated with the region specificity. This result suggests that epigenetic mechanisms are associated with astrocyte regional heterogeneity of gene expression. My findings contribute to understanding the diverse roles of transcription factors and epigenetic modulators for <italic>GFAP</italic> <italic>in vivo</italic> expression, and will help discovery of therapeutic targets for various CNS diseases involving altered <italic>GFAP</italic> expression.

PhD

1 online resource (vii, 80 pages) :illustrations

Ph.D.University of Alabama at Birmingham2012.

Neurobiology

Medicine

astrocytes, epigenetics, GFAP, regional heterogeneity, Transcription, transgenic mice

UNRESTRICTED

Advisors/Committee Members: Michael Brenner, Lubin,Farah Wilson,Scott Carroll, Steven L. Ryan, Thomas M..

Subjects/Keywords: Astrocytes – metabolism<; /br>; Brain Injuries – metabolism.<; /br>; Epigenesis, Genetic.<; /br>; Gene Expression Regulation – physiology<; /br>; Glial Fibrillary Acidic Protein – genetics.<; /br>; Mice, Transgenic<; /br>; Promoter Regions, Genetic – physiology<; /br>; Transcription Factors – metabolism

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

APA (6^th Edition):

Yeo, S. (2012). Transcriptional Regulation Of Gfap. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1661

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):

Yeo, Sujeong. “Transcriptional Regulation Of Gfap.” 2012. Thesis, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1661.

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

MLA Handbook (7^th Edition):

Yeo, Sujeong. “Transcriptional Regulation Of Gfap.” 2012. Web. 06 Mar 2021.

Vancouver:

Yeo S. Transcriptional Regulation Of Gfap. [Internet] [Thesis]. University of Alabama – Birmingham; 2012. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1661.

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

Council of Science Editors:

Yeo S. Transcriptional Regulation Of Gfap. [Thesis]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1661

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

Loma Linda University

18. Fukuda, Andrew Minoru. Role of Astrocyte Network in Edema after Juvenile Traumatic Brain Injury.

Degree: PhD, Basic Sciences, 2014, Loma Linda University

URL: https://scholarsrepository.llu.edu/etd/212

► Juvenile traumatic brain injury (jTBI) is the leading cause of death and disability in young children and adolescents. Despite its lasting detrimental effects on… (more)

▼ Juvenile traumatic brain injury (jTBI) is the leading cause of death and disability in young children and adolescents. Despite its lasting detrimental effects on the developing brain, no pharmacological treatment exists. One of the pathological hallmarks of jTBI is edema. Astrocytes play a key role in the edema process, and have been hypothesized that numerous astrocyte networks allow communication and propagation of edema and secondary injury spread. Two key astrocyte proteins are hypothesized to have a central role in the edema process: Aquaporin 4 (AQP4) and Connexin 43 (Cx43). AQP4 is expressed extensively in astrocyte endfeet, which surrounds the blood vessels as part of the blood brain barrier (BBB). Cx43 is central in astrocyte to astrocyte connection and communication. We hypothesized that AQP4 acted as one of the potential passageway of water into the astrocyte, whereas Cx43 acted as the bridge between astrocytes once inside the brain. By blocking these strategically located pathways, we hypothesized that edema would decrease post-jTBI. In order to achieve specific inhibitions of APQ4 or Cx43, we utilized small interference RNA (siRNA), which is also an endogenous mechanism. We observed that after jTBI both AQP4 and Cx43 was significantly upregulated, edema was prominent, and reactive astrogliosis occurred. When siAQP4 was administered after jTBI, there was functional improvement, decreased edema, and decreased reactive astrogliosis. When siCx43 was administered, there was functional improvement and decreased reactive astrogliosis, but the level of edema did not change. From these findings, it can be seen that (1) AQP4 and Cx43 are upregulated acutely after jTBI, (2) both siAQP4 and siCx43 have therapeutic potentials after jTBI leading to functional recovery, (3) although both target astrocyte endfeet proteins, the mechanism of action seem to be different and AQP4 may play a more direct role in the edema process than Cx43. Future studies could focus on (1) a more clinically relevant delivery of siRNA for jTBI, (2) elucidating the mechanism behind functional improvement of siCx43, and (3) the relationship between AQP4 and Cx43 regarding astrocyte pathology after jTBI. Advisors/Committee Members: Badaut, Jerome, Ashwal, Stephen, Candelario-Jalil, Eduardo, Oberg, Kerby, Zhang, John.

Subjects/Keywords: Anatomy; Medical Physiology; Medicine and Health Sciences; Musculoskeletal, Neural, and Ocular Physiology; Neurology; Neurosciences; Pediatrics; Brain Injuries - Physiopathology; Brain Edema - Physiopathology; Astrocytes - Metabolism; Aquaporins - Metabolism; Glial Fibrillary Acidic Protein; Juvenile Traumatic Brain Injury; jTBI; Edema; Connexin 43; Reactive Astrogliosis

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

APA (6^th Edition):

Fukuda, A. M. (2014). Role of Astrocyte Network in Edema after Juvenile Traumatic Brain Injury. (Doctoral Dissertation). Loma Linda University. Retrieved from https://scholarsrepository.llu.edu/etd/212

Chicago Manual of Style (16^th Edition):

Fukuda, Andrew Minoru. “Role of Astrocyte Network in Edema after Juvenile Traumatic Brain Injury.” 2014. Doctoral Dissertation, Loma Linda University. Accessed March 06, 2021. https://scholarsrepository.llu.edu/etd/212.

MLA Handbook (7^th Edition):

Fukuda, Andrew Minoru. “Role of Astrocyte Network in Edema after Juvenile Traumatic Brain Injury.” 2014. Web. 06 Mar 2021.

Vancouver:

Fukuda AM. Role of Astrocyte Network in Edema after Juvenile Traumatic Brain Injury. [Internet] [Doctoral dissertation]. Loma Linda University; 2014. [cited 2021 Mar 06]. Available from: https://scholarsrepository.llu.edu/etd/212.

Council of Science Editors:

Fukuda AM. Role of Astrocyte Network in Edema after Juvenile Traumatic Brain Injury. [Doctoral Dissertation]. Loma Linda University; 2014. Available from: https://scholarsrepository.llu.edu/etd/212

University of Missouri – Columbia

19. Hu, Chunhua. Activation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2.

Degree: 2007, University of Missouri – Columbia

URL: https://doi.org/10.32469/10355/6270

► [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Reactive oxygen species (ROS) are produced in cells by enzymic and non-enzymic mechanisms and play… (more)

Subjects/Keywords: Astrocytes; NAD (Coenzyme); Apoptosis; Cell membranes; Phospholipase A2 – Inhibitors; Cytosol; Oxidative stress; Active oxygen; Astrocytes – physiology; NADPH Oxidase – physiology; Apoptosis – physiology; Cell Membrane; Central Nervous System – physiology; NADP – antagonists & inhibitors; Oxidative Stress – physiology; Phospholipases A – metabolism; Reactive Oxygen Species – metabolism; Vitamin K3

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

APA (6^th Edition):

Hu, C. (2007). Activation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2. (Thesis). University of Missouri – Columbia. Retrieved from https://doi.org/10.32469/10355/6270

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):

Hu, Chunhua. “Activation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2.” 2007. Thesis, University of Missouri – Columbia. Accessed March 06, 2021. https://doi.org/10.32469/10355/6270.

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

MLA Handbook (7^th Edition):

Hu, Chunhua. “Activation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2.” 2007. Web. 06 Mar 2021.

Vancouver:

Hu C. Activation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2. [Internet] [Thesis]. University of Missouri – Columbia; 2007. [cited 2021 Mar 06]. Available from: https://doi.org/10.32469/10355/6270.

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

Council of Science Editors:

Hu C. Activation of astrocytes: involvement of NADPH oxidase and cytosolic phospholipase A2. [Thesis]. University of Missouri – Columbia; 2007. Available from: https://doi.org/10.32469/10355/6270

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

20. Gottipati, Manoj K. Modulation Of Morpho-Functional Characteristics Of Astrocytes Using Chemically-Functionalized Water-Soluble Single-Walled Carbon Nanotubes.

Degree: 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1469

►

In this thesis, I report the use of chemically functionalized water-soluble single-walled carbon nanotubes (ws-SWCNTs) for the modulation of morpho-functional characteristics of astrocytes. When added… (more)

Subjects/Keywords: Astrocytes.<; br>; Cells – Growth.<; br>; Cells – Morphology.<; br>; Cell physiology.<; br>; Nanotubes – Therapeutic use.<; br>; Nerve tissue – Wounds and injuries – Treatment.<; br>; Cytoplasmic filaments – Reactivity.

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APA (6^th Edition):

Gottipati, M. K. (2012). Modulation Of Morpho-Functional Characteristics Of Astrocytes Using Chemically-Functionalized Water-Soluble Single-Walled Carbon Nanotubes. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1469

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):

Gottipati, Manoj K. “Modulation Of Morpho-Functional Characteristics Of Astrocytes Using Chemically-Functionalized Water-Soluble Single-Walled Carbon Nanotubes.” 2012. Thesis, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1469.

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

MLA Handbook (7^th Edition):

Gottipati, Manoj K. “Modulation Of Morpho-Functional Characteristics Of Astrocytes Using Chemically-Functionalized Water-Soluble Single-Walled Carbon Nanotubes.” 2012. Web. 06 Mar 2021.

Vancouver:

Gottipati MK. Modulation Of Morpho-Functional Characteristics Of Astrocytes Using Chemically-Functionalized Water-Soluble Single-Walled Carbon Nanotubes. [Internet] [Thesis]. University of Alabama – Birmingham; 2012. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1469.

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

Council of Science Editors:

Gottipati MK. Modulation Of Morpho-Functional Characteristics Of Astrocytes Using Chemically-Functionalized Water-Soluble Single-Walled Carbon Nanotubes. [Thesis]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1469

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

21. McCoy, Eric. Expression and function of aquaporins in malignant and non-malignant astrocytes.

Degree: PhD, 2008, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,774

►

Aquaporins (AQP) constitute the primary pathway for water movement across cellular membrances. As a result, their expression and function are important for regulating cell volume.… (more)

▼

Aquaporins (AQP) constitute the primary pathway for water movement across cellular membrances. As a result, their expression and function are important for regulating cell volume. Both gliomas and astrocytes have highly effective volume regulatory mechanisms capable of rapidly moving ions and water into and out of cells following edemic episodes. In this dissertation, we examined the expression of AQPs in both gliomas and astrocytes in order to understand their function role as well as their regulation. We have shown that primary gliomas highly express AQP1 and AQP4 whereas cell lines express no AQP4 and variable AQP1. We reintroduced AQP1 and AQP4 into D54MG cell line lacking AQPs and examined their function. AQP1 enhanced tumor swelling and migration while AQP4 enhanced cell swelling and adhesion. PKC activation is known to regulate AQP function. Using PKC modulators, we found that while PKC did not regulate AQP1, AQP4 function was highly dependent on PKC activity. Specifically, phorbol 12-myristate 13-acetate, PKC activator, reduced cell swelling in AQP4-expressing tumors as well as migration. Chelerythrine, PKC inhibitor, enhanced both cell swelling and migration. Additionally, knocking out the PKC phosphorylation site at S180 eliminated the regulation of AQP4 water permeability and tumor migration. We verified this data by implanting AQP1, AQP4 and S180-AQP4 intracranially into mice and examined glioma invasion. We found that AQP1 and S180-AQP4 invaded on average significantly further than either AQP4 or control tumor cells lacking AQPs. AQP1 and S180-AQP4 invaded much further distances (>1500 μm) suggesting that AQP1 expressing tumors invade into tissue to set up satellite colonies characteristic of gliomas whereas AQP4 mediated invasion is regulated by PKC activity. Finally, we wanted to understand the regulation of AQP1 expression in astrocytes following injury. AQP1 is upregulated following cortical stab injury, and we could mimic this upregulation using an in vitro wound assay. We found that pMEK1/2 and pERK1/2 was increased up to 60 min post-injury but then subsequently decreased. AQP1 expression was increased by 16hrs. MEK1/2 and ERK1/2 activity as well as AQP1 expression was completely inhibited by U0126, a MAPK inhibitor. Astrocyte upregulation following injury is regulated by MAPK signaling.

1 online resource (x, 127 p. : ill., digital, PDF file)

Neurobiology

Joint Health Sciences

volume regulation tumor edema migration invasion cell signaling

UNRESTRICTED

Advisors/Committee Members: Sontheimer, Harald, Benos, Dale , Brenner, Michael , Wilson, Scott , Yoder, Bradley.

Subjects/Keywords: Aquaporin 1 Aquaporin 4<; br>; Aquaporins – metabolism<; br>; Astrocytes – physiology<; br>; Brain Injuries – physiopathology<; br>; Brain Neoplasms – metabolism<; br>; Cell Movement<; br>; Neoplasm Invasiveness<; br>; Wounds, Stab – physiopathology

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APA (6^th Edition):

McCoy, E. (2008). Expression and function of aquaporins in malignant and non-malignant astrocytes. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,774

Chicago Manual of Style (16^th Edition):

McCoy, Eric. “Expression and function of aquaporins in malignant and non-malignant astrocytes.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 06, 2021. http://contentdm.mhsl.uab.edu/u?/etd,774.

MLA Handbook (7^th Edition):

McCoy, Eric. “Expression and function of aquaporins in malignant and non-malignant astrocytes.” 2008. Web. 06 Mar 2021.

Vancouver:

McCoy E. Expression and function of aquaporins in malignant and non-malignant astrocytes. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Mar 06]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,774.

Council of Science Editors:

McCoy E. Expression and function of aquaporins in malignant and non-malignant astrocytes. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,774

Virginia Commonwealth University

22. Park, Sung H. High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules.

Degree: PhD, Physiology and Biophysics, 2016, Virginia Commonwealth University

URL: https://doi.org/10.25772/ACX8-TR69 ; https://scholarscompass.vcu.edu/etd/4433

► Ebselen (Ebs) is considered as a glutathione peroxidase (GPx) mimetic and primarily thought to function by scavenging intracellular reactive oxygen species (ROS). Previous to… (more)

Subjects/Keywords: Ebs; high affinity block of; DI TNC1 astrocytes; thiol-reactive small molecules; Ebs-p-yne; VRAC; Biophysics; Cellular and Molecular Physiology; Medicinal Chemistry and Pharmaceutics; Molecular and Cellular Neuroscience; Neuroscience and Neurobiology; Pharmacology, Toxicology and Environmental Health

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

APA (6^th Edition):

Park, S. H. (2016). High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/ACX8-TR69 ; https://scholarscompass.vcu.edu/etd/4433

Chicago Manual of Style (16^th Edition):

Park, Sung H. “High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules.” 2016. Doctoral Dissertation, Virginia Commonwealth University. Accessed March 06, 2021. https://doi.org/10.25772/ACX8-TR69 ; https://scholarscompass.vcu.edu/etd/4433.

MLA Handbook (7^th Edition):

Park, Sung H. “High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules.” 2016. Web. 06 Mar 2021.

Vancouver:

Park SH. High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2016. [cited 2021 Mar 06]. Available from: https://doi.org/10.25772/ACX8-TR69 ; https://scholarscompass.vcu.edu/etd/4433.

Council of Science Editors:

Park SH. High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules. [Doctoral Dissertation]. Virginia Commonwealth University; 2016. Available from: https://doi.org/10.25772/ACX8-TR69 ; https://scholarscompass.vcu.edu/etd/4433

Texas Medical Center

23. Vincent, Bryce H. The Role of the Androgen Receptor Cofactor p44/WDR77 in Astrocyte Activation.

Degree: PhD, 2011, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/134

► Astrogliosis is induced by neuronal damage and is also a pathological feature of the major aging-related neurodegenerative disorders. The mechanisms that control the cascade… (more)

▼ Astrogliosis is induced by neuronal damage and is also a pathological feature of the major aging-related neurodegenerative disorders. The mechanisms that control the cascade of astrogliosis have not been well established. In a previous study, we identified a novel androgen receptor (AR)-interacting protein (p44/WDR77) and found that it plays a critical role in the control of proliferation and differentiation of prostate epithelial cells. In the present study, we found that deletion of the p44 gene in the mouse brain caused accelerated aging with dramatic astrogliosis. The p44/WDR77 is expressed in astrocytes and loss of p44/WDR77 expression in astrocytes leads to astrogliosis. Our results reveal a novel role of p44/WDR77 in astrocytes, which may explain the well-documented role of androgens in suppression of astrogliosis. While many of detailed mechanisms of astrocyte activation remain to be elucidated, a number pathways have been implicated in astrocyte activation including p21^Cip1 and the NF-kB pathway. Astrocytic activation induced by p44/WDR77 gene deletion was associated with a significant increase of p21^Cip1 expression and NF-kB activation characterized by p65 nuclear localization. We found that down-regulation of p21^Cip1 expression inhibited astrocyte activation induced by the p44/WDR77 deletion and was accompanied by a decreased p65 nuclear localization. While p21^Cip1 role in astrocyte activation and NF-kB activation is not well understood, studies of other cell cycle regulators have implicated cell cycle control systems as modulators of astrocyte activation, thus p21^Cip1 could induce secondary effect to induce p65 nuclear localization. However, p65 knockdown completely relieved the inhibition of astrocyte growth induced by the p44/WDR77 deletion, while p21^Cip1 knockdown only partially recovered this inhibition. Thus, NF-kB activity performs additional regulatory actions not mediated by p21^Cip1. These analyses imply that p4/WDR77 suppresses astrocyte activation through modulating p21^Cip1 expressionand NF-kB activation. Advisors/Committee Members: Zhengxin Wang, Gary E. Gallick, Douglas Boyd.

Subjects/Keywords: p44; NF-kappa B; p21; astrocytes; androgen receptor; astrogliosis; Biochemistry; Cell Biology; Cellular and Molecular Physiology; Laboratory and Basic Science Research; Medical Biochemistry; Medical Neurobiology; Medical Sciences; Molecular and Cellular Neuroscience; Molecular Biology; Neurosciences

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APA (6^th Edition):

Vincent, B. H. (2011). The Role of the Androgen Receptor Cofactor p44/WDR77 in Astrocyte Activation. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/134

Chicago Manual of Style (16^th Edition):

Vincent, Bryce H. “The Role of the Androgen Receptor Cofactor p44/WDR77 in Astrocyte Activation.” 2011. Doctoral Dissertation, Texas Medical Center. Accessed March 06, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/134.

MLA Handbook (7^th Edition):

Vincent, Bryce H. “The Role of the Androgen Receptor Cofactor p44/WDR77 in Astrocyte Activation.” 2011. Web. 06 Mar 2021.

Vancouver:

Vincent BH. The Role of the Androgen Receptor Cofactor p44/WDR77 in Astrocyte Activation. [Internet] [Doctoral dissertation]. Texas Medical Center; 2011. [cited 2021 Mar 06]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/134.

Council of Science Editors:

Vincent BH. The Role of the Androgen Receptor Cofactor p44/WDR77 in Astrocyte Activation. [Doctoral Dissertation]. Texas Medical Center; 2011. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/134

University of Florida

24. Boyd, Frederick Tilghman, 1959-. Characterization and physiological significance of brain insulin receptors.

Degree: 1985, University of Florida

URL: https://ufdc.ufl.edu/AA00053670

Subjects/Keywords: Astrocytes; Brain; Cells; Cultured cells; Insulin; Neuroglia; Neurons; Norepinephrine; Rats; Receptors; Binding Sites ( mesh ); Brain Chemistry ( mesh ); Physiology thesis Ph.D ( mesh ); Receptor, Insulin – physiology ( mesh )

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

APA (6^th Edition):

Boyd, Frederick Tilghman, 1. (1985). Characterization and physiological significance of brain insulin receptors. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00053670

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):

Boyd, Frederick Tilghman, 1959-. “Characterization and physiological significance of brain insulin receptors.” 1985. Thesis, University of Florida. Accessed March 06, 2021. https://ufdc.ufl.edu/AA00053670.

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

MLA Handbook (7^th Edition):

Boyd, Frederick Tilghman, 1959-. “Characterization and physiological significance of brain insulin receptors.” 1985. Web. 06 Mar 2021.

Vancouver:

Boyd, Frederick Tilghman 1. Characterization and physiological significance of brain insulin receptors. [Internet] [Thesis]. University of Florida; 1985. [cited 2021 Mar 06]. Available from: https://ufdc.ufl.edu/AA00053670.

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

Council of Science Editors:

Boyd, Frederick Tilghman 1. Characterization and physiological significance of brain insulin receptors. [Thesis]. University of Florida; 1985. Available from: https://ufdc.ufl.edu/AA00053670

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

University of Florida

25. Olson, John Ackerman, 1964-. Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain.

Degree: 1990, University of Florida

URL: https://ufdc.ufl.edu/AA00022809

Subjects/Keywords: Astrocytes; Brain; Cell growth; Cells; Cultural studies; Cultured cells; Neurons; Rats; Receptors; Secretion; Angiotensin II – physiology ( mesh ); Astrocytes – growth &; development ( mesh ); Astrocytes – secretion ( mesh ); Brain Chemistry ( mesh ); Department of Pharmacology and Therapeutics thesis Ph.D ( mesh ); Insulin-Like Growth Factor-Binding Protein 2 ( mesh ); Proteins – secretion ( mesh ); Rats ( mesh ); Research ( mesh )

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APA (6^th Edition):

Olson, John Ackerman, 1. (1990). Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00022809

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):

Olson, John Ackerman, 1964-. “Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain.” 1990. Thesis, University of Florida. Accessed March 06, 2021. https://ufdc.ufl.edu/AA00022809.

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

MLA Handbook (7^th Edition):

Olson, John Ackerman, 1964-. “Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain.” 1990. Web. 06 Mar 2021.

Vancouver:

Olson, John Ackerman 1. Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain. [Internet] [Thesis]. University of Florida; 1990. [cited 2021 Mar 06]. Available from: https://ufdc.ufl.edu/AA00022809.

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

Council of Science Editors:

Olson, John Ackerman 1. Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain. [Thesis]. University of Florida; 1990. Available from: https://ufdc.ufl.edu/AA00022809

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

26. Augustine, Claudia. Traumatic Injury in vitro Elicits JNK-mediated Human Astrocyte Retraction, but Spares Cerebrovascular Endothelial Cells.

Degree: 2013, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/1411

► The pathophysiology of a traumatic brain injury (TBI) involves the dysfunction of the blood-brain barrier (BBB). The lumen of the BBB is lined with cerebrovascular… (more)

Subjects/Keywords: traumatic brain injury; human astrocytes; human cerebrovascular endothelial cells; blood-brain barrier; MAP kinases; cellular retraction; Physiology

…Dehydrogenase GDNF Glial-derived Neurotrophic Factor HA Human Astrocytes HRP Horseradish… …astrocytes, with smaller numbers of pericytes, and pericytic macrophages [3]. These cells… …Perivascular astrocytes project their specialized endfeet to surround the cerebral microvasculature… …perivascular astrocytes. Together, they function to infer a low permeability of the blood vessel and… …Perivascular astrocytes project their endfeet to almost entirely cover the basolateral side of the…

12 more images…

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APA (6^th Edition):

Augustine, C. (2013). Traumatic Injury in vitro Elicits JNK-mediated Human Astrocyte Retraction, but Spares Cerebrovascular Endothelial Cells. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/1411

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):

Augustine, Claudia. “Traumatic Injury in vitro Elicits JNK-mediated Human Astrocyte Retraction, but Spares Cerebrovascular Endothelial Cells.” 2013. Thesis, University of Western Ontario. Accessed March 06, 2021. https://ir.lib.uwo.ca/etd/1411.

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

MLA Handbook (7^th Edition):

Augustine, Claudia. “Traumatic Injury in vitro Elicits JNK-mediated Human Astrocyte Retraction, but Spares Cerebrovascular Endothelial Cells.” 2013. Web. 06 Mar 2021.

Vancouver:

Augustine C. Traumatic Injury in vitro Elicits JNK-mediated Human Astrocyte Retraction, but Spares Cerebrovascular Endothelial Cells. [Internet] [Thesis]. University of Western Ontario; 2013. [cited 2021 Mar 06]. Available from: https://ir.lib.uwo.ca/etd/1411.

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

Council of Science Editors:

Augustine C. Traumatic Injury in vitro Elicits JNK-mediated Human Astrocyte Retraction, but Spares Cerebrovascular Endothelial Cells. [Thesis]. University of Western Ontario; 2013. Available from: https://ir.lib.uwo.ca/etd/1411

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

University of Florida

27. Paulding, Waltke Reche, 1964-. Regulation of atrial natriuretic peptide receptors in astroglia.

Degree: 1996, University of Florida

URL: https://ufdc.ufl.edu/AA00067432

Subjects/Keywords: Research ( mesh ); Receptors, Atrial Natriuretic Factor – physiology ( mesh ); Astrocytes ( mesh ); Cells, Cultured ( mesh ); Protein Kinase C – physiology ( mesh ); Angiotensin II – physiology ( mesh ); Rats, Sprague-Dawley ( mesh ); Rats, Inbred SHR ( mesh ); Rats, Inbred WKY ( mesh ); Department of Physiology thesis Ph.D ( mesh )

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APA (6^th Edition):

Paulding, Waltke Reche, 1. (1996). Regulation of atrial natriuretic peptide receptors in astroglia. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00067432

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):

Paulding, Waltke Reche, 1964-. “Regulation of atrial natriuretic peptide receptors in astroglia.” 1996. Thesis, University of Florida. Accessed March 06, 2021. https://ufdc.ufl.edu/AA00067432.

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

MLA Handbook (7^th Edition):

Paulding, Waltke Reche, 1964-. “Regulation of atrial natriuretic peptide receptors in astroglia.” 1996. Web. 06 Mar 2021.

Vancouver:

Paulding, Waltke Reche 1. Regulation of atrial natriuretic peptide receptors in astroglia. [Internet] [Thesis]. University of Florida; 1996. [cited 2021 Mar 06]. Available from: https://ufdc.ufl.edu/AA00067432.

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

Council of Science Editors:

Paulding, Waltke Reche 1. Regulation of atrial natriuretic peptide receptors in astroglia. [Thesis]. University of Florida; 1996. Available from: https://ufdc.ufl.edu/AA00067432

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

University of Florida

28. Rydzewski, Bartosz, 1967-. Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system.

Degree: 1992, University of Florida

URL: https://ufdc.ufl.edu/AA00066134

Subjects/Keywords: Research ( mesh ); Angiotensin II – physiology ( mesh ); Angiotensin II – pharmacology ( mesh ); Protease Inhibitors – metabolism ( mesh ); Plasminogen Activator Inhibitor 1 – metabolism ( mesh ); RNA, Messenger – metabolism ( mesh ); Central Nervous System – physiology ( mesh ); Gene Expression Regulation ( mesh ); Rats, Inbred WKY ( mesh ); Astrocytes ( mesh ); Brain – physiology ( mesh ); Department of Physiology thesis Ph.D ( mesh )

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

APA (6^th Edition):

Rydzewski, Bartosz, 1. (1992). Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00066134

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):

Rydzewski, Bartosz, 1967-. “Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system.” 1992. Thesis, University of Florida. Accessed March 06, 2021. https://ufdc.ufl.edu/AA00066134.

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

MLA Handbook (7^th Edition):

Rydzewski, Bartosz, 1967-. “Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system.” 1992. Web. 06 Mar 2021.

Vancouver:

Rydzewski, Bartosz 1. Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system. [Internet] [Thesis]. University of Florida; 1992. [cited 2021 Mar 06]. Available from: https://ufdc.ufl.edu/AA00066134.

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

Council of Science Editors:

Rydzewski, Bartosz 1. Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system. [Thesis]. University of Florida; 1992. Available from: https://ufdc.ufl.edu/AA00066134

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

University of Florida

29. Masters, Brian Andrew, 1962-. Insulin-like growth factors in cell differentiation and development in the nervous system.

Degree: 1990, University of Florida

URL: https://ufdc.ufl.edu/AA00056906

Subjects/Keywords: Astrocytes; Brain; Cultured cells; Insulin; Neurons; Oligodendroglia; Progenitor cells; Rats; Receptors; Somatomedins; Department of Physiology thesis Ph.D ( mesh ); Insulin-Like Growth Factor I ( mesh ); Nervous System – growth &; development ( mesh ); Oligodendroglia ( mesh ); Receptors, Somatomedin ( mesh ); Research ( mesh )

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

APA (6^th Edition):

Masters, Brian Andrew, 1. (1990). Insulin-like growth factors in cell differentiation and development in the nervous system. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00056906

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):

Masters, Brian Andrew, 1962-. “Insulin-like growth factors in cell differentiation and development in the nervous system.” 1990. Thesis, University of Florida. Accessed March 06, 2021. https://ufdc.ufl.edu/AA00056906.

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

MLA Handbook (7^th Edition):

Masters, Brian Andrew, 1962-. “Insulin-like growth factors in cell differentiation and development in the nervous system.” 1990. Web. 06 Mar 2021.

Vancouver:

Masters, Brian Andrew 1. Insulin-like growth factors in cell differentiation and development in the nervous system. [Internet] [Thesis]. University of Florida; 1990. [cited 2021 Mar 06]. Available from: https://ufdc.ufl.edu/AA00056906.

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

Council of Science Editors:

Masters, Brian Andrew 1. Insulin-like growth factors in cell differentiation and development in the nervous system. [Thesis]. University of Florida; 1990. Available from: https://ufdc.ufl.edu/AA00056906

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

University of Florida

30. Reutter, Michael A., 1959-. Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter.

Degree: 1997, University of Florida

URL: https://ufdc.ufl.edu/AA00011813

Subjects/Keywords: Adrenergic receptors; Agonists; Astrocytes; Cell lines; Cultured cells; Inurement; Messenger RNA; Norepinephrine; Rats; Receptors; Angiotensin II ( mesh ); Astrocytes ( mesh ); Cells, Cultured ( mesh ); Cyclic AMP ( mesh ); Department of Physiology thesis Ph.D ( mesh ); Epinephrine ( mesh ); Gene Expression Regulation ( mesh ); Protein Kinase C ( mesh ); RNA, Messenger ( mesh ); Rats, Sprague-Dawley ( mesh ); Receptors, Adrenergic, alpha-2 – biosynthesis ( mesh ); Receptors, Adrenergic, alpha-2 – metabolism ( mesh ); Research ( mesh ); Signal Transduction ( mesh ); Transcription, Genetic ( mesh )

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APA (6^th Edition):

Reutter, Michael A., 1. (1997). Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00011813

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):

Reutter, Michael A., 1959-. “Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter.” 1997. Thesis, University of Florida. Accessed March 06, 2021. https://ufdc.ufl.edu/AA00011813.

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

MLA Handbook (7^th Edition):

Reutter, Michael A., 1959-. “Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter.” 1997. Web. 06 Mar 2021.

Vancouver:

Reutter, Michael A. 1. Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter. [Internet] [Thesis]. University of Florida; 1997. [cited 2021 Mar 06]. Available from: https://ufdc.ufl.edu/AA00011813.

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

Council of Science Editors:

Reutter, Michael A. 1. Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter. [Thesis]. University of Florida; 1997. Available from: https://ufdc.ufl.edu/AA00011813

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

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