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You searched for +publisher:"Vanderbilt University" +contributor:("Robert L. Macdonald"). Showing records 1 – 10 of 10 total matches.

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Vanderbilt University

1. Shen, Dingding. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.

Degree: PhD, Neuroscience, 2017, Vanderbilt University

 Epileptic encephalopathies (EEs) are a devastating group of severe childhood onset epilepsies with medication resistant seizures and poor developmental outcomes. Many EEs have a genetic… (more)

Subjects/Keywords: Epileptic encephalopathies; GABAA receptor

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APA (6th Edition):

Shen, D. (2017). Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14271

Chicago Manual of Style (16th Edition):

Shen, Dingding. “Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.” 2017. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/14271.

MLA Handbook (7th Edition):

Shen, Dingding. “Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.” 2017. Web. 16 Jan 2021.

Vancouver:

Shen D. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. [Internet] [Doctoral dissertation]. Vanderbilt University; 2017. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/14271.

Council of Science Editors:

Shen D. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. [Doctoral Dissertation]. Vanderbilt University; 2017. Available from: http://hdl.handle.net/1803/14271


Vanderbilt University

2. Arain, Fazal Manzoor. Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Epilepsy is a disease characterized by two or more unprovoked seizures. Two mutations, S326fs328X and A322D, in the α1 subunit of GABAA receptor (Gabra1), are… (more)

Subjects/Keywords: GABA; Epilepsy; Development

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APA (6th Edition):

Arain, F. M. (2014). Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10463

Chicago Manual of Style (16th Edition):

Arain, Fazal Manzoor. “Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/10463.

MLA Handbook (7th Edition):

Arain, Fazal Manzoor. “Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice.” 2014. Web. 16 Jan 2021.

Vancouver:

Arain FM. Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/10463.

Council of Science Editors:

Arain FM. Two Human Epilepsy Mutations Cause Developmentally Dependant Changes in Seizure Phenotype and GABAA Receptor Expression in Genetically Modified Mice. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/10463


Vanderbilt University

3. Satpute Janve, Vaishali. Epileptic encephalopathy associated human GABRB mutations disrupt GABAA receptor function and results in Lennox-Gastaut syndrome in Gabrb3+/D120N knock-in mice.

Degree: PhD, Neuroscience, 2019, Vanderbilt University

 Epileptic encephalopathies (EEs) are catastrophic childhood epilepsies with intractable seizures, developmental delays, and cognitive impairment. I determined the functional impact of five de novo GABAA… (more)

Subjects/Keywords: mouse model; pediatric; Epilepsy; GABAA receptor mutations; Lennox-Gastaut syndrome

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APA (6th Edition):

Satpute Janve, V. (2019). Epileptic encephalopathy associated human GABRB mutations disrupt GABAA receptor function and results in Lennox-Gastaut syndrome in Gabrb3+/D120N knock-in mice. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11950

Chicago Manual of Style (16th Edition):

Satpute Janve, Vaishali. “Epileptic encephalopathy associated human GABRB mutations disrupt GABAA receptor function and results in Lennox-Gastaut syndrome in Gabrb3+/D120N knock-in mice.” 2019. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/11950.

MLA Handbook (7th Edition):

Satpute Janve, Vaishali. “Epileptic encephalopathy associated human GABRB mutations disrupt GABAA receptor function and results in Lennox-Gastaut syndrome in Gabrb3+/D120N knock-in mice.” 2019. Web. 16 Jan 2021.

Vancouver:

Satpute Janve V. Epileptic encephalopathy associated human GABRB mutations disrupt GABAA receptor function and results in Lennox-Gastaut syndrome in Gabrb3+/D120N knock-in mice. [Internet] [Doctoral dissertation]. Vanderbilt University; 2019. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/11950.

Council of Science Editors:

Satpute Janve V. Epileptic encephalopathy associated human GABRB mutations disrupt GABAA receptor function and results in Lennox-Gastaut syndrome in Gabrb3+/D120N knock-in mice. [Doctoral Dissertation]. Vanderbilt University; 2019. Available from: http://hdl.handle.net/1803/11950


Vanderbilt University

4. Huang, Xuan. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Epilepsy is a neurological disorder affecting almost one percent of the population, and genetic epilepsy are those caused by a presumed or unknown genetic factor(s).… (more)

Subjects/Keywords: GABA(A) receptors; GABRG2; genetic epilepsy; mutation; therapy

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APA (6th Edition):

Huang, X. (2014). Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14755

Chicago Manual of Style (16th Edition):

Huang, Xuan. “Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/14755.

MLA Handbook (7th Edition):

Huang, Xuan. “Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.” 2014. Web. 16 Jan 2021.

Vancouver:

Huang X. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/14755.

Council of Science Editors:

Huang X. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14755


Vanderbilt University

5. Tang, Xin. Modulation of GABAA receptor function by PKA and PKC protein phosphorylation.

Degree: PhD, Neuroscience, 2010, Vanderbilt University

 We studied the modulation of ¦Á4¦Â3¦Ã2L and ¦Á4¦Â3¦Ä GABAA receptor currents by two protein kinases, PKA and PKC. Although modulation of synaptic ¦Á1¦Â¦Ã2 GABAA receptor… (more)

Subjects/Keywords: PKC; GABAA receptor; phosphorylation; PKA

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APA (6th Edition):

Tang, X. (2010). Modulation of GABAA receptor function by PKA and PKC protein phosphorylation. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11843

Chicago Manual of Style (16th Edition):

Tang, Xin. “Modulation of GABAA receptor function by PKA and PKC protein phosphorylation.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/11843.

MLA Handbook (7th Edition):

Tang, Xin. “Modulation of GABAA receptor function by PKA and PKC protein phosphorylation.” 2010. Web. 16 Jan 2021.

Vancouver:

Tang X. Modulation of GABAA receptor function by PKA and PKC protein phosphorylation. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/11843.

Council of Science Editors:

Tang X. Modulation of GABAA receptor function by PKA and PKC protein phosphorylation. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11843


Vanderbilt University

6. Lo, Wen-yi. Structural determinants of GABAA receptor biogenesis.

Degree: PhD, Neuroscience, 2008, Vanderbilt University

 This project is concerned with identifying and characterizing structural determinants of GABAA receptor biogenesis. I used flow cytometry to measure surface levels of GABAA receptor… (more)

Subjects/Keywords: PNGaseF; blocking forward trafficking; sucrose density gradient; endo H

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APA (6th Edition):

Lo, W. (2008). Structural determinants of GABAA receptor biogenesis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14766

Chicago Manual of Style (16th Edition):

Lo, Wen-yi. “Structural determinants of GABAA receptor biogenesis.” 2008. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/14766.

MLA Handbook (7th Edition):

Lo, Wen-yi. “Structural determinants of GABAA receptor biogenesis.” 2008. Web. 16 Jan 2021.

Vancouver:

Lo W. Structural determinants of GABAA receptor biogenesis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2008. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/14766.

Council of Science Editors:

Lo W. Structural determinants of GABAA receptor biogenesis. [Doctoral Dissertation]. Vanderbilt University; 2008. Available from: http://hdl.handle.net/1803/14766


Vanderbilt University

7. Botzolakis, Emmanuel John. Kinetic Determinants of GABA-A Receptor Function.

Degree: PhD, Neuroscience, 2010, Vanderbilt University

 GABA-A receptors are ligand-gated chloride channels that mediate the majority of fast inhibitory signaling in the central nervous system. Their kinetic properties determine the charge… (more)

Subjects/Keywords: kinetics; modeling; desensitization; deactivation; electrophysiology; patch clamp; ion channel; GABA

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APA (6th Edition):

Botzolakis, E. J. (2010). Kinetic Determinants of GABA-A Receptor Function. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11865

Chicago Manual of Style (16th Edition):

Botzolakis, Emmanuel John. “Kinetic Determinants of GABA-A Receptor Function.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/11865.

MLA Handbook (7th Edition):

Botzolakis, Emmanuel John. “Kinetic Determinants of GABA-A Receptor Function.” 2010. Web. 16 Jan 2021.

Vancouver:

Botzolakis EJ. Kinetic Determinants of GABA-A Receptor Function. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/11865.

Council of Science Editors:

Botzolakis EJ. Kinetic Determinants of GABA-A Receptor Function. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11865


Vanderbilt University

8. Zhu, Lei. KCC2 and NKCC1 in the control of neuronal Cl- and brain excitability.

Degree: PhD, Neuroscience, 2007, Vanderbilt University

 During postnatal development of the central nervous system, the response of GABAA receptor to its agonist undergoes a switch from excitatory to inhibitory, due to… (more)

Subjects/Keywords: Neural transmission  – Regulation; GABA; NKCC1; KCC2; Cotransporters; Chlorides  – Physiological transport; Brain  – Growth

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APA (6th Edition):

Zhu, L. (2007). KCC2 and NKCC1 in the control of neuronal Cl- and brain excitability. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13769

Chicago Manual of Style (16th Edition):

Zhu, Lei. “KCC2 and NKCC1 in the control of neuronal Cl- and brain excitability.” 2007. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/13769.

MLA Handbook (7th Edition):

Zhu, Lei. “KCC2 and NKCC1 in the control of neuronal Cl- and brain excitability.” 2007. Web. 16 Jan 2021.

Vancouver:

Zhu L. KCC2 and NKCC1 in the control of neuronal Cl- and brain excitability. [Internet] [Doctoral dissertation]. Vanderbilt University; 2007. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/13769.

Council of Science Editors:

Zhu L. KCC2 and NKCC1 in the control of neuronal Cl- and brain excitability. [Doctoral Dissertation]. Vanderbilt University; 2007. Available from: http://hdl.handle.net/1803/13769


Vanderbilt University

9. Byun, Nellie Eunjoo. Disruption of the K-Cl Cotransporter-3 Leads to Severe Peripheral Neuropathy.

Degree: PhD, Neuroscience, 2008, Vanderbilt University

 Mutations in the human K-Cl cotransporter-3 (KCC3) gene lead to a severe neurological disorder called peripheral neuropathy associated with agenesis of the corpus callosum (ACCPN).… (more)

Subjects/Keywords: cell volume regulation; peripheral neuropathy; Sciatic nerve  – Pathophysiology; Andermann syndrome; KCC3; ACCPN; cation chloride cotransporter; Nerves Peripheral  – Diseases  – Etiology; Chlorides  – Physiological transport

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APA (6th Edition):

Byun, N. E. (2008). Disruption of the K-Cl Cotransporter-3 Leads to Severe Peripheral Neuropathy. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/15272

Chicago Manual of Style (16th Edition):

Byun, Nellie Eunjoo. “Disruption of the K-Cl Cotransporter-3 Leads to Severe Peripheral Neuropathy.” 2008. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/15272.

MLA Handbook (7th Edition):

Byun, Nellie Eunjoo. “Disruption of the K-Cl Cotransporter-3 Leads to Severe Peripheral Neuropathy.” 2008. Web. 16 Jan 2021.

Vancouver:

Byun NE. Disruption of the K-Cl Cotransporter-3 Leads to Severe Peripheral Neuropathy. [Internet] [Doctoral dissertation]. Vanderbilt University; 2008. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/15272.

Council of Science Editors:

Byun NE. Disruption of the K-Cl Cotransporter-3 Leads to Severe Peripheral Neuropathy. [Doctoral Dissertation]. Vanderbilt University; 2008. Available from: http://hdl.handle.net/1803/15272


Vanderbilt University

10. Misra, Sunita N. Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy.

Degree: PhD, Pharmacology, 2008, Vanderbilt University

 Investigating genetic forms of epilepsy allows for improved understanding of epilepsy pathophysiology in general. Mutations in voltage-gated sodium channels are a frequent cause of genetic… (more)

Subjects/Keywords: Sodium channels  – Pathophysiology; electrophysiology; epilepsy; Epilepsy  – Genetic aspects; Epilepsy  – Molecular aspects

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APA (6th Edition):

Misra, S. N. (2008). Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12753

Chicago Manual of Style (16th Edition):

Misra, Sunita N. “Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy.” 2008. Doctoral Dissertation, Vanderbilt University. Accessed January 16, 2021. http://hdl.handle.net/1803/12753.

MLA Handbook (7th Edition):

Misra, Sunita N. “Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy.” 2008. Web. 16 Jan 2021.

Vancouver:

Misra SN. Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy. [Internet] [Doctoral dissertation]. Vanderbilt University; 2008. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1803/12753.

Council of Science Editors:

Misra SN. Characterization of Mutant Human Brain Sodium Channels Associated with Familial Epilepsy. [Doctoral Dissertation]. Vanderbilt University; 2008. Available from: http://hdl.handle.net/1803/12753

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