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You searched for subject:(Excitotoxicity). Showing records 1 – 30 of 121 total matches.

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University of Alberta

1. Dhami, Kamaldeep S. The effects of antidepressants on the phenotype of activated microglia and ischemia-injured cortical neurons.

Degree: PhD, Centre for Neuroscience, 2013, University of Alberta

 Depression is one of the most common disorders appearing following a stroke and is also a major factor limiting recovery and rehabilitation in stroke patients.… (more)

Subjects/Keywords: Inflammation; Microglia; Excitotoxicity; Ischemia; Antidepressants

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APA (6th Edition):

Dhami, K. S. (2013). The effects of antidepressants on the phenotype of activated microglia and ischemia-injured cortical neurons. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/5x21tf82p

Chicago Manual of Style (16th Edition):

Dhami, Kamaldeep S. “The effects of antidepressants on the phenotype of activated microglia and ischemia-injured cortical neurons.” 2013. Doctoral Dissertation, University of Alberta. Accessed October 27, 2020. https://era.library.ualberta.ca/files/5x21tf82p.

MLA Handbook (7th Edition):

Dhami, Kamaldeep S. “The effects of antidepressants on the phenotype of activated microglia and ischemia-injured cortical neurons.” 2013. Web. 27 Oct 2020.

Vancouver:

Dhami KS. The effects of antidepressants on the phenotype of activated microglia and ischemia-injured cortical neurons. [Internet] [Doctoral dissertation]. University of Alberta; 2013. [cited 2020 Oct 27]. Available from: https://era.library.ualberta.ca/files/5x21tf82p.

Council of Science Editors:

Dhami KS. The effects of antidepressants on the phenotype of activated microglia and ischemia-injured cortical neurons. [Doctoral Dissertation]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/5x21tf82p


University of Melbourne

2. Hossain, Mohammed Iqbal. Investigating the role of c-Src in excitotoxic neuronal death.

Degree: 2012, University of Melbourne

 Glutamate-induced excitotoxicity is a major cause of neuronal loss in acute neural injury such as cerebral ischemic stroke and neurotrauma. Additionally, it also contributes to… (more)

Subjects/Keywords: excitotoxicity; stroke; neuronal death

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APA (6th Edition):

Hossain, M. I. (2012). Investigating the role of c-Src in excitotoxic neuronal death. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37398

Chicago Manual of Style (16th Edition):

Hossain, Mohammed Iqbal. “Investigating the role of c-Src in excitotoxic neuronal death.” 2012. Doctoral Dissertation, University of Melbourne. Accessed October 27, 2020. http://hdl.handle.net/11343/37398.

MLA Handbook (7th Edition):

Hossain, Mohammed Iqbal. “Investigating the role of c-Src in excitotoxic neuronal death.” 2012. Web. 27 Oct 2020.

Vancouver:

Hossain MI. Investigating the role of c-Src in excitotoxic neuronal death. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/11343/37398.

Council of Science Editors:

Hossain MI. Investigating the role of c-Src in excitotoxic neuronal death. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37398


University of Melbourne

3. JOHANSSEN, TIMOTHY. The Role of metals and Aβ in excitotoxicity and Alzheimer’s disease.

Degree: 2015, University of Melbourne

 Background: N-methyl-d-aspartate receptors (NMDARs) are ionotropic channels gated by the excitatory amino acid, glutamate. They play an essential role in synaptic plasticity, enhancing synaptic signal… (more)

Subjects/Keywords: Alzheimer's disease; beta amyloid; excitotoxicity

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APA (6th Edition):

JOHANSSEN, T. (2015). The Role of metals and Aβ in excitotoxicity and Alzheimer’s disease. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/55550

Chicago Manual of Style (16th Edition):

JOHANSSEN, TIMOTHY. “The Role of metals and Aβ in excitotoxicity and Alzheimer’s disease.” 2015. Doctoral Dissertation, University of Melbourne. Accessed October 27, 2020. http://hdl.handle.net/11343/55550.

MLA Handbook (7th Edition):

JOHANSSEN, TIMOTHY. “The Role of metals and Aβ in excitotoxicity and Alzheimer’s disease.” 2015. Web. 27 Oct 2020.

Vancouver:

JOHANSSEN T. The Role of metals and Aβ in excitotoxicity and Alzheimer’s disease. [Internet] [Doctoral dissertation]. University of Melbourne; 2015. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/11343/55550.

Council of Science Editors:

JOHANSSEN T. The Role of metals and Aβ in excitotoxicity and Alzheimer’s disease. [Doctoral Dissertation]. University of Melbourne; 2015. Available from: http://hdl.handle.net/11343/55550


University of New South Wales

4. Bi, Mian. Genetic Factors in Excitotoxicity and Stroke.

Degree: Medical Sciences, 2018, University of New South Wales

Excitotoxicity refers to the damaging and toxic effects inflicted upon neuronal tissue resulting from excessive or prolonged activation of excitatory receptors. It has been implicated… (more)

Subjects/Keywords: Tau; Excitotoxicity; Stroke; Seizure

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APA (6th Edition):

Bi, M. (2018). Genetic Factors in Excitotoxicity and Stroke. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/60043 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51124/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Bi, Mian. “Genetic Factors in Excitotoxicity and Stroke.” 2018. Doctoral Dissertation, University of New South Wales. Accessed October 27, 2020. http://handle.unsw.edu.au/1959.4/60043 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51124/SOURCE02?view=true.

MLA Handbook (7th Edition):

Bi, Mian. “Genetic Factors in Excitotoxicity and Stroke.” 2018. Web. 27 Oct 2020.

Vancouver:

Bi M. Genetic Factors in Excitotoxicity and Stroke. [Internet] [Doctoral dissertation]. University of New South Wales; 2018. [cited 2020 Oct 27]. Available from: http://handle.unsw.edu.au/1959.4/60043 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51124/SOURCE02?view=true.

Council of Science Editors:

Bi M. Genetic Factors in Excitotoxicity and Stroke. [Doctoral Dissertation]. University of New South Wales; 2018. Available from: http://handle.unsw.edu.au/1959.4/60043 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:51124/SOURCE02?view=true


University of Rochester

5. Fahrenthold, Berkeley Kristyn. Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury.

Degree: PhD, 2017, University of Rochester

Excitotoxicity leads to disruption of the intracellular environment and activation of cytotoxic cascades that cause neuronal death. Multiple cell types, including both neurons and glia,… (more)

Subjects/Keywords: Retina; Excitotoxicity; NMDA; TNF; JNK; CHOP

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APA (6th Edition):

Fahrenthold, B. K. (2017). Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/32924

Chicago Manual of Style (16th Edition):

Fahrenthold, Berkeley Kristyn. “Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury.” 2017. Doctoral Dissertation, University of Rochester. Accessed October 27, 2020. http://hdl.handle.net/1802/32924.

MLA Handbook (7th Edition):

Fahrenthold, Berkeley Kristyn. “Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury.” 2017. Web. 27 Oct 2020.

Vancouver:

Fahrenthold BK. Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury. [Internet] [Doctoral dissertation]. University of Rochester; 2017. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/1802/32924.

Council of Science Editors:

Fahrenthold BK. Assessment of the Involvement of Intrinsic and Extrinsic Cell Death Pathways in Retinal Ganglion Cell Death after Excitotoxic Injury. [Doctoral Dissertation]. University of Rochester; 2017. Available from: http://hdl.handle.net/1802/32924


Vanderbilt University

6. Gibson, Chelsea Lynn. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.

Degree: PhD, Neuroscience, 2018, Vanderbilt University

 Glutamate (Glu) signaling plays a critical role in regulating neural excitability, thus supporting many behaviors. Perturbed Glu homeostasis in the brain is implicated in multiple… (more)

Subjects/Keywords: C. elegans; dopamine; glia; glutamate; excitotoxicity; neurodegeneration

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APA (6th Edition):

Gibson, C. L. (2018). Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11175

Chicago Manual of Style (16th Edition):

Gibson, Chelsea Lynn. “Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed October 27, 2020. http://hdl.handle.net/1803/11175.

MLA Handbook (7th Edition):

Gibson, Chelsea Lynn. “Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.” 2018. Web. 27 Oct 2020.

Vancouver:

Gibson CL. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/1803/11175.

Council of Science Editors:

Gibson CL. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/11175


Universiteit Utrecht

7. Kerkhofs, A. Prenatal stress and the NMDA receptor.

Degree: 2012, Universiteit Utrecht

 Early adversity, including prenatal stress (PS), is a prevalent problem in our modern world. The affected unborn child experiences severe problems later in life, such… (more)

Subjects/Keywords: Prenatal stress; NMDA; corticosterone; dendritic morphology; neurogenesis; excitotoxicity; NR2A; NR2B

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APA (6th Edition):

Kerkhofs, A. (2012). Prenatal stress and the NMDA receptor. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/248894

Chicago Manual of Style (16th Edition):

Kerkhofs, A. “Prenatal stress and the NMDA receptor.” 2012. Masters Thesis, Universiteit Utrecht. Accessed October 27, 2020. http://dspace.library.uu.nl:8080/handle/1874/248894.

MLA Handbook (7th Edition):

Kerkhofs, A. “Prenatal stress and the NMDA receptor.” 2012. Web. 27 Oct 2020.

Vancouver:

Kerkhofs A. Prenatal stress and the NMDA receptor. [Internet] [Masters thesis]. Universiteit Utrecht; 2012. [cited 2020 Oct 27]. Available from: http://dspace.library.uu.nl:8080/handle/1874/248894.

Council of Science Editors:

Kerkhofs A. Prenatal stress and the NMDA receptor. [Masters Thesis]. Universiteit Utrecht; 2012. Available from: http://dspace.library.uu.nl:8080/handle/1874/248894


McMaster University

8. Knoch, Jaime. The role of resting mast cells in the survival of myenteric neurons.

Degree: MSc, 2019, McMaster University

The enteric nervous system (ENS) is an incredibly complex neural network that is extensively integrated within the neuroimmunoendocrine system through countless signalling pathways that have… (more)

Subjects/Keywords: Enteric nervous system; Mast cells; Myenteric plexus; BMMC; Excitotoxicity; Kynurenine Pathway

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APA (6th Edition):

Knoch, J. (2019). The role of resting mast cells in the survival of myenteric neurons. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/24938

Chicago Manual of Style (16th Edition):

Knoch, Jaime. “The role of resting mast cells in the survival of myenteric neurons.” 2019. Masters Thesis, McMaster University. Accessed October 27, 2020. http://hdl.handle.net/11375/24938.

MLA Handbook (7th Edition):

Knoch, Jaime. “The role of resting mast cells in the survival of myenteric neurons.” 2019. Web. 27 Oct 2020.

Vancouver:

Knoch J. The role of resting mast cells in the survival of myenteric neurons. [Internet] [Masters thesis]. McMaster University; 2019. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/11375/24938.

Council of Science Editors:

Knoch J. The role of resting mast cells in the survival of myenteric neurons. [Masters Thesis]. McMaster University; 2019. Available from: http://hdl.handle.net/11375/24938


University of Toronto

9. McCutcheon, Victoria Elizabeth. Characterization and Validation of Two Zebrafish Models of Traumatic Brain Injury (TBI).

Degree: 2015, University of Toronto

Traumatic brain injury (TBI) is a leading cause of death and morbidity in industrialized countries. The cost and time associated with pre-clinical development of TBI… (more)

Subjects/Keywords: Excitotoxicity; Modelling; Neuroprotection; Secondary Injury; Traumatic Brain Injury; Zebrafish; 0317

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APA (6th Edition):

McCutcheon, V. E. (2015). Characterization and Validation of Two Zebrafish Models of Traumatic Brain Injury (TBI). (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/70457

Chicago Manual of Style (16th Edition):

McCutcheon, Victoria Elizabeth. “Characterization and Validation of Two Zebrafish Models of Traumatic Brain Injury (TBI).” 2015. Masters Thesis, University of Toronto. Accessed October 27, 2020. http://hdl.handle.net/1807/70457.

MLA Handbook (7th Edition):

McCutcheon, Victoria Elizabeth. “Characterization and Validation of Two Zebrafish Models of Traumatic Brain Injury (TBI).” 2015. Web. 27 Oct 2020.

Vancouver:

McCutcheon VE. Characterization and Validation of Two Zebrafish Models of Traumatic Brain Injury (TBI). [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/1807/70457.

Council of Science Editors:

McCutcheon VE. Characterization and Validation of Two Zebrafish Models of Traumatic Brain Injury (TBI). [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/70457


University of the Western Cape

10. Abaniwonda, Modupe. Polycyclic compounds as carriers for neuroactive non- steroidal anti-inflammatory drugs .

Degree: 2017, University of the Western Cape

 Recent scientific findings have highlighted the beneficial roles of polycyclic cage compounds in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. Further interest into the… (more)

Subjects/Keywords: Neurodegenerative disorders; Oxidative stress; Excitotoxicity; Polycyclic cage compounds; Blood-brain barrier

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APA (6th Edition):

Abaniwonda, M. (2017). Polycyclic compounds as carriers for neuroactive non- steroidal anti-inflammatory drugs . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/5693

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

Chicago Manual of Style (16th Edition):

Abaniwonda, Modupe. “Polycyclic compounds as carriers for neuroactive non- steroidal anti-inflammatory drugs .” 2017. Thesis, University of the Western Cape. Accessed October 27, 2020. http://hdl.handle.net/11394/5693.

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

MLA Handbook (7th Edition):

Abaniwonda, Modupe. “Polycyclic compounds as carriers for neuroactive non- steroidal anti-inflammatory drugs .” 2017. Web. 27 Oct 2020.

Vancouver:

Abaniwonda M. Polycyclic compounds as carriers for neuroactive non- steroidal anti-inflammatory drugs . [Internet] [Thesis]. University of the Western Cape; 2017. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/11394/5693.

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

Council of Science Editors:

Abaniwonda M. Polycyclic compounds as carriers for neuroactive non- steroidal anti-inflammatory drugs . [Thesis]. University of the Western Cape; 2017. Available from: http://hdl.handle.net/11394/5693

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


University of Manchester

11. Bray, Natasha. IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity.

Degree: 2013, University of Manchester

 Neuroinflammation is a major driver of secondary brain cell death after ischaemic stroke, seizure activity and traumatic brain injury. In a model of excitotoxic neuroinflammation,… (more)

Subjects/Keywords: haemodynamic response; neuroinflammation; excitotoxicity; interleukin-1; optical imaging spectroscopy

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APA (6th Edition):

Bray, N. (2013). IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:213705

Chicago Manual of Style (16th Edition):

Bray, Natasha. “IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity.” 2013. Doctoral Dissertation, University of Manchester. Accessed October 27, 2020. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:213705.

MLA Handbook (7th Edition):

Bray, Natasha. “IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity.” 2013. Web. 27 Oct 2020.

Vancouver:

Bray N. IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2020 Oct 27]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:213705.

Council of Science Editors:

Bray N. IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity. [Doctoral Dissertation]. University of Manchester; 2013. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:213705


University of Miami

12. Johnstone, Joshua T. Astrocyte-Mediated Oligodendrocyte Death Following Spinal Cord Injury: Glutamate, Zinc, and Oligodendrocyte-NADPH Oxidase Dependent Mechanisms.

Degree: PhD, Neuroscience (Medicine), 2011, University of Miami

 Spinal cord injury (SCI) often results in irreversible paralysis and widespread oligodendrocyte death and white matter damage. While the mechanisms underlying this phenomenon are poorly… (more)

Subjects/Keywords: Oligodendrocyte; NADPH oxidase; zinc; astrocyte; spinal cord injury; excitotoxicity

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APA (6th Edition):

Johnstone, J. T. (2011). Astrocyte-Mediated Oligodendrocyte Death Following Spinal Cord Injury: Glutamate, Zinc, and Oligodendrocyte-NADPH Oxidase Dependent Mechanisms. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/638

Chicago Manual of Style (16th Edition):

Johnstone, Joshua T. “Astrocyte-Mediated Oligodendrocyte Death Following Spinal Cord Injury: Glutamate, Zinc, and Oligodendrocyte-NADPH Oxidase Dependent Mechanisms.” 2011. Doctoral Dissertation, University of Miami. Accessed October 27, 2020. https://scholarlyrepository.miami.edu/oa_dissertations/638.

MLA Handbook (7th Edition):

Johnstone, Joshua T. “Astrocyte-Mediated Oligodendrocyte Death Following Spinal Cord Injury: Glutamate, Zinc, and Oligodendrocyte-NADPH Oxidase Dependent Mechanisms.” 2011. Web. 27 Oct 2020.

Vancouver:

Johnstone JT. Astrocyte-Mediated Oligodendrocyte Death Following Spinal Cord Injury: Glutamate, Zinc, and Oligodendrocyte-NADPH Oxidase Dependent Mechanisms. [Internet] [Doctoral dissertation]. University of Miami; 2011. [cited 2020 Oct 27]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/638.

Council of Science Editors:

Johnstone JT. Astrocyte-Mediated Oligodendrocyte Death Following Spinal Cord Injury: Glutamate, Zinc, and Oligodendrocyte-NADPH Oxidase Dependent Mechanisms. [Doctoral Dissertation]. University of Miami; 2011. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/638


University of Manitoba

13. Hunt, Waylon T. Effects of PARP-1 signaling and conjugated linoleic acid on brain cell bioenergetics and survival.

Degree: Pharmacology and Therapeutics, 2010, University of Manitoba

 Glutamate is the primary excitatory neurotransmitter in the central nervous system. Extracellular glutamate concentrations are tightly regulated to avoid over-stimulation of glutamate receptors, which leads… (more)

Subjects/Keywords: CLA; Neurons; bioenergetics; PARP-1; Astrocytes; Stroke; Alzheimer's; excitotoxicity

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APA (6th Edition):

Hunt, W. T. (2010). Effects of PARP-1 signaling and conjugated linoleic acid on brain cell bioenergetics and survival. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/5070

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

Chicago Manual of Style (16th Edition):

Hunt, Waylon T. “Effects of PARP-1 signaling and conjugated linoleic acid on brain cell bioenergetics and survival.” 2010. Thesis, University of Manitoba. Accessed October 27, 2020. http://hdl.handle.net/1993/5070.

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

MLA Handbook (7th Edition):

Hunt, Waylon T. “Effects of PARP-1 signaling and conjugated linoleic acid on brain cell bioenergetics and survival.” 2010. Web. 27 Oct 2020.

Vancouver:

Hunt WT. Effects of PARP-1 signaling and conjugated linoleic acid on brain cell bioenergetics and survival. [Internet] [Thesis]. University of Manitoba; 2010. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/1993/5070.

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

Council of Science Editors:

Hunt WT. Effects of PARP-1 signaling and conjugated linoleic acid on brain cell bioenergetics and survival. [Thesis]. University of Manitoba; 2010. Available from: http://hdl.handle.net/1993/5070

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


University of Manchester

14. Bray, Natasha. IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity.

Degree: PhD, 2013, University of Manchester

 Neuroinflammation is a major driver of secondary brain cell death after ischaemic stroke, seizure activity and traumatic brain injury. In a model of excitotoxic neuroinflammation,… (more)

Subjects/Keywords: 570; haemodynamic response; neuroinflammation; excitotoxicity; interleukin-1; optical imaging spectroscopy

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

APA (6th Edition):

Bray, N. (2013). IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/il1mediated-changes-in-cerebral-perfusion-and-neural-activity-in-a-rat-model-of-neuroinflammation-and-excitotoxicity(f9784ec8-0438-4d3c-aef1-b56a9b86ac01).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.764272

Chicago Manual of Style (16th Edition):

Bray, Natasha. “IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity.” 2013. Doctoral Dissertation, University of Manchester. Accessed October 27, 2020. https://www.research.manchester.ac.uk/portal/en/theses/il1mediated-changes-in-cerebral-perfusion-and-neural-activity-in-a-rat-model-of-neuroinflammation-and-excitotoxicity(f9784ec8-0438-4d3c-aef1-b56a9b86ac01).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.764272.

MLA Handbook (7th Edition):

Bray, Natasha. “IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity.” 2013. Web. 27 Oct 2020.

Vancouver:

Bray N. IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2020 Oct 27]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/il1mediated-changes-in-cerebral-perfusion-and-neural-activity-in-a-rat-model-of-neuroinflammation-and-excitotoxicity(f9784ec8-0438-4d3c-aef1-b56a9b86ac01).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.764272.

Council of Science Editors:

Bray N. IL-1β-mediated changes in cerebral perfusion and neural activity in a rat model of neuroinflammation and excitotoxicity. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/il1mediated-changes-in-cerebral-perfusion-and-neural-activity-in-a-rat-model-of-neuroinflammation-and-excitotoxicity(f9784ec8-0438-4d3c-aef1-b56a9b86ac01).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.764272

15. Doyle, Seán P. Excitotoxic injury mechanisms in central white matter.

Degree: PhD, 2017, University of Plymouth

 Myelinated axons are crucial for rapid information transmission within the central nervous system (CNS). Myelin injury is a common feature of white matter (WM) pathology… (more)

Subjects/Keywords: 616.8; White matter; Myelin; Stroke; Glutamate; Excitotoxicity; Vesicles; Axon; Electrophysiology; Ischemia

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APA (6th Edition):

Doyle, S. P. (2017). Excitotoxic injury mechanisms in central white matter. (Doctoral Dissertation). University of Plymouth. Retrieved from http://hdl.handle.net/10026.1/9586

Chicago Manual of Style (16th Edition):

Doyle, Seán P. “Excitotoxic injury mechanisms in central white matter.” 2017. Doctoral Dissertation, University of Plymouth. Accessed October 27, 2020. http://hdl.handle.net/10026.1/9586.

MLA Handbook (7th Edition):

Doyle, Seán P. “Excitotoxic injury mechanisms in central white matter.” 2017. Web. 27 Oct 2020.

Vancouver:

Doyle SP. Excitotoxic injury mechanisms in central white matter. [Internet] [Doctoral dissertation]. University of Plymouth; 2017. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/10026.1/9586.

Council of Science Editors:

Doyle SP. Excitotoxic injury mechanisms in central white matter. [Doctoral Dissertation]. University of Plymouth; 2017. Available from: http://hdl.handle.net/10026.1/9586


University of Melbourne

16. Kamaruddin, Mohd Aizuddin. Novel peptide-based approaches to study the activity and substrate specificity of protein kinases.

Degree: 2013, University of Melbourne

 Protein phosphorylation, catalyzed by protein kinases, is the predominant post-translational modification made to proteins. This process is readily reversible, with protein phosphatases catalyzing removal of… (more)

Subjects/Keywords: protein kinases; fluorescence; phosphorescence; lanthanides; Src; CHK; excitotoxicity

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APA (6th Edition):

Kamaruddin, M. A. (2013). Novel peptide-based approaches to study the activity and substrate specificity of protein kinases. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38062

Chicago Manual of Style (16th Edition):

Kamaruddin, Mohd Aizuddin. “Novel peptide-based approaches to study the activity and substrate specificity of protein kinases.” 2013. Doctoral Dissertation, University of Melbourne. Accessed October 27, 2020. http://hdl.handle.net/11343/38062.

MLA Handbook (7th Edition):

Kamaruddin, Mohd Aizuddin. “Novel peptide-based approaches to study the activity and substrate specificity of protein kinases.” 2013. Web. 27 Oct 2020.

Vancouver:

Kamaruddin MA. Novel peptide-based approaches to study the activity and substrate specificity of protein kinases. [Internet] [Doctoral dissertation]. University of Melbourne; 2013. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/11343/38062.

Council of Science Editors:

Kamaruddin MA. Novel peptide-based approaches to study the activity and substrate specificity of protein kinases. [Doctoral Dissertation]. University of Melbourne; 2013. Available from: http://hdl.handle.net/11343/38062


University of Melbourne

17. HOQUE, MD ASHFAQUL. Exploring the signalling mechanism of excitotoxic neuronal injury by molecular and quantitative proteomic approaches.

Degree: 2016, University of Melbourne

Excitotoxicity caused by over-stimulation of the ionotropic glutamate receptors is a key neuronal cell death process underpinning brain damage in acute and chronic neurological disorders… (more)

Subjects/Keywords: Excitotoxicity; neurons; NMDA receptors; proteomic analysis; phosphoproteomic analysis

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APA (6th Edition):

HOQUE, M. A. (2016). Exploring the signalling mechanism of excitotoxic neuronal injury by molecular and quantitative proteomic approaches. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/113673

Chicago Manual of Style (16th Edition):

HOQUE, MD ASHFAQUL. “Exploring the signalling mechanism of excitotoxic neuronal injury by molecular and quantitative proteomic approaches.” 2016. Doctoral Dissertation, University of Melbourne. Accessed October 27, 2020. http://hdl.handle.net/11343/113673.

MLA Handbook (7th Edition):

HOQUE, MD ASHFAQUL. “Exploring the signalling mechanism of excitotoxic neuronal injury by molecular and quantitative proteomic approaches.” 2016. Web. 27 Oct 2020.

Vancouver:

HOQUE MA. Exploring the signalling mechanism of excitotoxic neuronal injury by molecular and quantitative proteomic approaches. [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/11343/113673.

Council of Science Editors:

HOQUE MA. Exploring the signalling mechanism of excitotoxic neuronal injury by molecular and quantitative proteomic approaches. [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/113673

18. Emnett, Christine Marie. Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events.

Degree: PhD, Biology & Biomedical Sciences (Neurosciences), 2014, Washington University in St. Louis

  N-methyl-D-aspartate receptors (NMDARs) are ionotropic glutamate receptors that serve crucial signaling and neurotrophic functions throughout the central nervous system. Both hyperfunction and hypofunction of… (more)

Subjects/Keywords: 24-S hydroxycholesterol; anti-depressants; channel block; excitotoxicity; ketamine; memantine; Biology

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APA (6th Edition):

Emnett, C. M. (2014). Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/347

Chicago Manual of Style (16th Edition):

Emnett, Christine Marie. “Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events.” 2014. Doctoral Dissertation, Washington University in St. Louis. Accessed October 27, 2020. https://openscholarship.wustl.edu/art_sci_etds/347.

MLA Handbook (7th Edition):

Emnett, Christine Marie. “Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events.” 2014. Web. 27 Oct 2020.

Vancouver:

Emnett CM. Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2014. [cited 2020 Oct 27]. Available from: https://openscholarship.wustl.edu/art_sci_etds/347.

Council of Science Editors:

Emnett CM. Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events. [Doctoral Dissertation]. Washington University in St. Louis; 2014. Available from: https://openscholarship.wustl.edu/art_sci_etds/347

19. Edokpolo, Anthony Omorodion. Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration.

Degree: MS(M.S.), Biology, 2014, City University of New York

Excitotoxicity is an important and frequently observed neurodegenerative process. Excitotoxicity mediates brain damage in a range of diseases and conditions including stroke, and is… (more)

Subjects/Keywords: Excitotoxicity; genetic screens; neurodegeneration; Biology; Cell and Developmental Biology

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APA (6th Edition):

Edokpolo, A. O. (2014). Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration. (Thesis). City University of New York. Retrieved from https://academicworks.cuny.edu/cc_etds_theses/516

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

Chicago Manual of Style (16th Edition):

Edokpolo, Anthony Omorodion. “Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration.” 2014. Thesis, City University of New York. Accessed October 27, 2020. https://academicworks.cuny.edu/cc_etds_theses/516.

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

MLA Handbook (7th Edition):

Edokpolo, Anthony Omorodion. “Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration.” 2014. Web. 27 Oct 2020.

Vancouver:

Edokpolo AO. Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration. [Internet] [Thesis]. City University of New York; 2014. [cited 2020 Oct 27]. Available from: https://academicworks.cuny.edu/cc_etds_theses/516.

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

Council of Science Editors:

Edokpolo AO. Screen for Suppressors and Enhancers of Excitotoxic Neurodegeneration. [Thesis]. City University of New York; 2014. Available from: https://academicworks.cuny.edu/cc_etds_theses/516

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


Arizona State University

20. Liu, Qiang. A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation.

Degree: PhD, Neuroscience, 2011, Arizona State University

 Patients with Alzheimer's disease (AD) exhibit a significantly higher incidence of unprovoked seizures compared to age-matched non-AD controls, and animal models of AD (i.e., transgenic… (more)

Subjects/Keywords: Neurosciences; amyloid; excitotoxicity; hyperexcitation; nicotinic receptor; patch clamp

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APA (6th Edition):

Liu, Q. (2011). A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation. (Doctoral Dissertation). Arizona State University. Retrieved from http://repository.asu.edu/items/9108

Chicago Manual of Style (16th Edition):

Liu, Qiang. “A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation.” 2011. Doctoral Dissertation, Arizona State University. Accessed October 27, 2020. http://repository.asu.edu/items/9108.

MLA Handbook (7th Edition):

Liu, Qiang. “A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation.” 2011. Web. 27 Oct 2020.

Vancouver:

Liu Q. A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation. [Internet] [Doctoral dissertation]. Arizona State University; 2011. [cited 2020 Oct 27]. Available from: http://repository.asu.edu/items/9108.

Council of Science Editors:

Liu Q. A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation. [Doctoral Dissertation]. Arizona State University; 2011. Available from: http://repository.asu.edu/items/9108


Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

21. Stamoula, Eleni. Πειραματική μελέτη της μοριακής απάντησης νευρικών κυττάρων μετά από τοξικότητα εκ διεγέρσεως (διεγερσιμοτοξικότητα) από γλουταμινικό οξύ.

Degree: 2016, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

Glutamate is a potent neurotransmitter that regulates various physiological functions such as learning, memory, long term potentiation and synaptic plasticity. Increasing amounts of glutamate are… (more)

Subjects/Keywords: Γλουταμινικό οξύ; Διεγερσιμοτοξικότητα; Αυτοφαγία; Μοριακές συνοδοί; Glutamate; Excitotoxicity; Autophagy; Molecular chaperone

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APA (6th Edition):

Stamoula, E. (2016). Πειραματική μελέτη της μοριακής απάντησης νευρικών κυττάρων μετά από τοξικότητα εκ διεγέρσεως (διεγερσιμοτοξικότητα) από γλουταμινικό οξύ. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/38188

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

Chicago Manual of Style (16th Edition):

Stamoula, Eleni. “Πειραματική μελέτη της μοριακής απάντησης νευρικών κυττάρων μετά από τοξικότητα εκ διεγέρσεως (διεγερσιμοτοξικότητα) από γλουταμινικό οξύ.” 2016. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed October 27, 2020. http://hdl.handle.net/10442/hedi/38188.

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

MLA Handbook (7th Edition):

Stamoula, Eleni. “Πειραματική μελέτη της μοριακής απάντησης νευρικών κυττάρων μετά από τοξικότητα εκ διεγέρσεως (διεγερσιμοτοξικότητα) από γλουταμινικό οξύ.” 2016. Web. 27 Oct 2020.

Vancouver:

Stamoula E. Πειραματική μελέτη της μοριακής απάντησης νευρικών κυττάρων μετά από τοξικότητα εκ διεγέρσεως (διεγερσιμοτοξικότητα) από γλουταμινικό οξύ. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2016. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/10442/hedi/38188.

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

Council of Science Editors:

Stamoula E. Πειραματική μελέτη της μοριακής απάντησης νευρικών κυττάρων μετά από τοξικότητα εκ διεγέρσεως (διεγερσιμοτοξικότητα) από γλουταμινικό οξύ. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2016. Available from: http://hdl.handle.net/10442/hedi/38188

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


University of British Columbia

22. Lo, Edmund. The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons.

Degree: MS- MSc, Neuroscience, 2007, University of British Columbia

 Stroke is a pathological condition that causes extensive brain damage. During ischemic stroke, an excess of the excitatory neurotransmitter glutamate exerts many deleterious effects, which… (more)

Subjects/Keywords: stroke; peptide; excitotoxicity; Calpain; Tat

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

APA (6th Edition):

Lo, E. (2007). The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons. (Masters Thesis). University of British Columbia. Retrieved from http://hdl.handle.net/2429/233

Chicago Manual of Style (16th Edition):

Lo, Edmund. “The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons.” 2007. Masters Thesis, University of British Columbia. Accessed October 27, 2020. http://hdl.handle.net/2429/233.

MLA Handbook (7th Edition):

Lo, Edmund. “The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons.” 2007. Web. 27 Oct 2020.

Vancouver:

Lo E. The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons. [Internet] [Masters thesis]. University of British Columbia; 2007. [cited 2020 Oct 27]. Available from: http://hdl.handle.net/2429/233.

Council of Science Editors:

Lo E. The development of a method to deliver neuroprotective peptides specifically into stroke-affected neurons. [Masters Thesis]. University of British Columbia; 2007. Available from: http://hdl.handle.net/2429/233


University of New South Wales

23. Stayte, Sandy. The preclinical investigations of inflammation and excitotoxicity in mouse models of Parkinson's disease.

Degree: Garvan Institute of Medical Research, 2015, University of New South Wales

 Parkinson’s disease (PD) is a neurodegenerative disorder that manifests as a result of degeneration of the nigrostriatal system. While L-Dopa still remains the most effective… (more)

Subjects/Keywords: Excitotoxicity; Parkinson's disease; Inflammation; Activin A; Kainate receptors; MPTP; 6-OHDA

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APA (6th Edition):

Stayte, S. (2015). The preclinical investigations of inflammation and excitotoxicity in mouse models of Parkinson's disease. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55108 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36544/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Stayte, Sandy. “The preclinical investigations of inflammation and excitotoxicity in mouse models of Parkinson's disease.” 2015. Doctoral Dissertation, University of New South Wales. Accessed October 27, 2020. http://handle.unsw.edu.au/1959.4/55108 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36544/SOURCE02?view=true.

MLA Handbook (7th Edition):

Stayte, Sandy. “The preclinical investigations of inflammation and excitotoxicity in mouse models of Parkinson's disease.” 2015. Web. 27 Oct 2020.

Vancouver:

Stayte S. The preclinical investigations of inflammation and excitotoxicity in mouse models of Parkinson's disease. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2020 Oct 27]. Available from: http://handle.unsw.edu.au/1959.4/55108 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36544/SOURCE02?view=true.

Council of Science Editors:

Stayte S. The preclinical investigations of inflammation and excitotoxicity in mouse models of Parkinson's disease. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55108 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:36544/SOURCE02?view=true


University of New South Wales

24. Gorlamandala, Naga Rajesh. The contribution of canonical transient receptor potential (TRPC) ion channels to ischemic brain injury.

Degree: Medical Sciences, 2017, University of New South Wales

 Ischemic brain injury is the third leading cause of mortality and the leading cause of disability in Australia. However, there are no neuroprotective treatments to… (more)

Subjects/Keywords: Glutamate excitotoxicity; Transient receptor potential canonical; Ischemia; Neuronal death

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APA (6th Edition):

Gorlamandala, N. R. (2017). The contribution of canonical transient receptor potential (TRPC) ion channels to ischemic brain injury. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/57396 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:43360/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Gorlamandala, Naga Rajesh. “The contribution of canonical transient receptor potential (TRPC) ion channels to ischemic brain injury.” 2017. Doctoral Dissertation, University of New South Wales. Accessed October 27, 2020. http://handle.unsw.edu.au/1959.4/57396 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:43360/SOURCE02?view=true.

MLA Handbook (7th Edition):

Gorlamandala, Naga Rajesh. “The contribution of canonical transient receptor potential (TRPC) ion channels to ischemic brain injury.” 2017. Web. 27 Oct 2020.

Vancouver:

Gorlamandala NR. The contribution of canonical transient receptor potential (TRPC) ion channels to ischemic brain injury. [Internet] [Doctoral dissertation]. University of New South Wales; 2017. [cited 2020 Oct 27]. Available from: http://handle.unsw.edu.au/1959.4/57396 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:43360/SOURCE02?view=true.

Council of Science Editors:

Gorlamandala NR. The contribution of canonical transient receptor potential (TRPC) ion channels to ischemic brain injury. [Doctoral Dissertation]. University of New South Wales; 2017. Available from: http://handle.unsw.edu.au/1959.4/57396 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:43360/SOURCE02?view=true


University of Cincinnati

25. Isom, Amanda M. The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia.

Degree: PhD, Medicine: Neuroscience/Medical Science Scholars Interdisciplinary, 2014, University of Cincinnati

 An estimated 35 million diabetic patients worldwide take antipsychotic medications for a variety of co-morbid mental illnesses. Diabetic patients frequently experience hypoglycemic episodes ranging from… (more)

Subjects/Keywords: Neurology; excitotoxicity; microglia; antipsychotic; haloperidol; quetiapine; cell death

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APA (6th Edition):

Isom, A. M. (2014). The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1407407111

Chicago Manual of Style (16th Edition):

Isom, Amanda M. “The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia.” 2014. Doctoral Dissertation, University of Cincinnati. Accessed October 27, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1407407111.

MLA Handbook (7th Edition):

Isom, Amanda M. “The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia.” 2014. Web. 27 Oct 2020.

Vancouver:

Isom AM. The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia. [Internet] [Doctoral dissertation]. University of Cincinnati; 2014. [cited 2020 Oct 27]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1407407111.

Council of Science Editors:

Isom AM. The Cellular Consequences of Combining Antipsychotic Medications and Hypoglycemia. [Doctoral Dissertation]. University of Cincinnati; 2014. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1407407111


The Ohio State University

26. Miller, Brandon Andrew. The effects of excitotoxicity and microglial activation on oligodendrocyte survival.

Degree: PhD, Neuroscience, 2007, The Ohio State University

 The nervous system transmits information over long distances by action potentials carried by neurons. In both the central and peripheral nervous system, neurons are insulated… (more)

Subjects/Keywords: oligodendrocyte; microglia; excitotoxicity; inflammation

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APA (6th Edition):

Miller, B. A. (2007). The effects of excitotoxicity and microglial activation on oligodendrocyte survival. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1177537595

Chicago Manual of Style (16th Edition):

Miller, Brandon Andrew. “The effects of excitotoxicity and microglial activation on oligodendrocyte survival.” 2007. Doctoral Dissertation, The Ohio State University. Accessed October 27, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1177537595.

MLA Handbook (7th Edition):

Miller, Brandon Andrew. “The effects of excitotoxicity and microglial activation on oligodendrocyte survival.” 2007. Web. 27 Oct 2020.

Vancouver:

Miller BA. The effects of excitotoxicity and microglial activation on oligodendrocyte survival. [Internet] [Doctoral dissertation]. The Ohio State University; 2007. [cited 2020 Oct 27]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1177537595.

Council of Science Editors:

Miller BA. The effects of excitotoxicity and microglial activation on oligodendrocyte survival. [Doctoral Dissertation]. The Ohio State University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1177537595


University of Pennsylvania

27. O'donnell, John Charles. Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions.

Degree: 2016, University of Pennsylvania

 ABSTRACT GLUTAMATE TRANSPORT AFFECTS MITOCHONDRIA AND CALCIUM SIGNALING IN ASTROCYTIC PROCESSES UNDER NORMAL AND PATHOLOGICAL CONDITIONS John Charles O’Donnell Michael B. Robinson Mitochondria are responsible… (more)

Subjects/Keywords: astrocytes; calcium; excitotoxicity; glutamate transport; mitochondria; stroke; Neuroscience and Neurobiology; Pharmacology

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APA (6th Edition):

O'donnell, J. C. (2016). Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/2504

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

Chicago Manual of Style (16th Edition):

O'donnell, John Charles. “Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions.” 2016. Thesis, University of Pennsylvania. Accessed October 27, 2020. https://repository.upenn.edu/edissertations/2504.

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

MLA Handbook (7th Edition):

O'donnell, John Charles. “Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions.” 2016. Web. 27 Oct 2020.

Vancouver:

O'donnell JC. Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions. [Internet] [Thesis]. University of Pennsylvania; 2016. [cited 2020 Oct 27]. Available from: https://repository.upenn.edu/edissertations/2504.

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

Council of Science Editors:

O'donnell JC. Glutamate Transport Affects Mitochondria And Calcium Signaling In Astrocytic Processes Under Normal And Pathological Conditions. [Thesis]. University of Pennsylvania; 2016. Available from: https://repository.upenn.edu/edissertations/2504

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


University of Kentucky

28. Berry, Jennifer Nicole. TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION.

Degree: 2010, University of Kentucky

Excitotoxicity is the overexcitation of neurons due to the excessive activation of excitatory amino acid receptors and is thought to be involved in many neurodegenerative… (more)

Subjects/Keywords: NMDA Receptors; Excitotoxicity; NR1 subunit; Synaptophysin; Topographical nature of death following excitotoxicity; Psychology

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APA (6th Edition):

Berry, J. N. (2010). TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION. (Masters Thesis). University of Kentucky. Retrieved from https://uknowledge.uky.edu/gradschool_theses/72

Chicago Manual of Style (16th Edition):

Berry, Jennifer Nicole. “TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION.” 2010. Masters Thesis, University of Kentucky. Accessed October 27, 2020. https://uknowledge.uky.edu/gradschool_theses/72.

MLA Handbook (7th Edition):

Berry, Jennifer Nicole. “TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION.” 2010. Web. 27 Oct 2020.

Vancouver:

Berry JN. TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION. [Internet] [Masters thesis]. University of Kentucky; 2010. [cited 2020 Oct 27]. Available from: https://uknowledge.uky.edu/gradschool_theses/72.

Council of Science Editors:

Berry JN. TIME-DEPENDENCE OF DISTAL-TO-PROXIMAL HIPPOCAMPAL NEURODEGENERATION PRODUCED BY N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION. [Masters Thesis]. University of Kentucky; 2010. Available from: https://uknowledge.uky.edu/gradschool_theses/72


University of California – San Diego

29. Chen, PeiXi. Spontaneous Neurogenic Electromyographic Activities in ALS G93A Rats, Potential Over-Excitatory Drive Leading to Alpha Motor Neuron Degeneration.

Degree: Biology, 2018, University of California – San Diego

 Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by a progressive degeneration of alpha-motor neurons, which results in motor-ambulatory and respiratory dysfunction. One… (more)

Subjects/Keywords: Neurosciences; ALS; Electromyographic Recordings; Excitotoxicity; Primary Afferents; Spinal Intermediate Zone; Spontaneous Neurogenic Activities

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

APA (6th Edition):

Chen, P. (2018). Spontaneous Neurogenic Electromyographic Activities in ALS G93A Rats, Potential Over-Excitatory Drive Leading to Alpha Motor Neuron Degeneration. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/2273c11n

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

Chicago Manual of Style (16th Edition):

Chen, PeiXi. “Spontaneous Neurogenic Electromyographic Activities in ALS G93A Rats, Potential Over-Excitatory Drive Leading to Alpha Motor Neuron Degeneration.” 2018. Thesis, University of California – San Diego. Accessed October 27, 2020. http://www.escholarship.org/uc/item/2273c11n.

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

MLA Handbook (7th Edition):

Chen, PeiXi. “Spontaneous Neurogenic Electromyographic Activities in ALS G93A Rats, Potential Over-Excitatory Drive Leading to Alpha Motor Neuron Degeneration.” 2018. Web. 27 Oct 2020.

Vancouver:

Chen P. Spontaneous Neurogenic Electromyographic Activities in ALS G93A Rats, Potential Over-Excitatory Drive Leading to Alpha Motor Neuron Degeneration. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2020 Oct 27]. Available from: http://www.escholarship.org/uc/item/2273c11n.

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

Council of Science Editors:

Chen P. Spontaneous Neurogenic Electromyographic Activities in ALS G93A Rats, Potential Over-Excitatory Drive Leading to Alpha Motor Neuron Degeneration. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/2273c11n

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


Michigan Technological University

30. Behnke, Jessica. ELEVATED L-LACTATE DRIVES MAJOR CELLULAR PATHOLOGIES ASSOCIATED WITH NEURODEGENERATION.

Degree: MS, Department of Biological Sciences, 2018, Michigan Technological University

  Within the past few decades, lactate research has expanded from initial findings deeming lactate as a dead-end metabolic product to recognition of lactate’s role… (more)

Subjects/Keywords: lactate; neurodegeneration; oxidative stress; mitochondrial dysfunction; excitotoxicity; Biological Factors; Nervous System Diseases

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

APA (6th Edition):

Behnke, J. (2018). ELEVATED L-LACTATE DRIVES MAJOR CELLULAR PATHOLOGIES ASSOCIATED WITH NEURODEGENERATION. (Masters Thesis). Michigan Technological University. Retrieved from http://digitalcommons.mtu.edu/etdr/564

Chicago Manual of Style (16th Edition):

Behnke, Jessica. “ELEVATED L-LACTATE DRIVES MAJOR CELLULAR PATHOLOGIES ASSOCIATED WITH NEURODEGENERATION.” 2018. Masters Thesis, Michigan Technological University. Accessed October 27, 2020. http://digitalcommons.mtu.edu/etdr/564.

MLA Handbook (7th Edition):

Behnke, Jessica. “ELEVATED L-LACTATE DRIVES MAJOR CELLULAR PATHOLOGIES ASSOCIATED WITH NEURODEGENERATION.” 2018. Web. 27 Oct 2020.

Vancouver:

Behnke J. ELEVATED L-LACTATE DRIVES MAJOR CELLULAR PATHOLOGIES ASSOCIATED WITH NEURODEGENERATION. [Internet] [Masters thesis]. Michigan Technological University; 2018. [cited 2020 Oct 27]. Available from: http://digitalcommons.mtu.edu/etdr/564.

Council of Science Editors:

Behnke J. ELEVATED L-LACTATE DRIVES MAJOR CELLULAR PATHOLOGIES ASSOCIATED WITH NEURODEGENERATION. [Masters Thesis]. Michigan Technological University; 2018. Available from: http://digitalcommons.mtu.edu/etdr/564

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