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You searched for +publisher:"University of Texas – Austin" +contributor:("Raab-Graham, Kimberly F."). Showing records 1 – 5 of 5 total matches.

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University of Texas – Austin

1. Wolfe, Sarah Anne. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.

Degree: PhD, Cellular and Molecular Biology, 2017, University of Texas – Austin

 Alcohol Use Disorder (AUD) and Major Depressive Disorder (MDD) are two widespread and debilitating disorders that share a high rate of comorbidity with the presence… (more)

Subjects/Keywords: Alcohol use disorder; Major depressive disorder; Ethanol; Rapid antidepressants; FMRP; GABABR; Ro 25-6981; RNA-sequencing; Synaptoneurosomes; Exon usage

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APA (6th Edition):

Wolfe, S. A. (2017). Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/2231

Chicago Manual of Style (16th Edition):

Wolfe, Sarah Anne. “Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.” 2017. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://dx.doi.org/10.26153/tsw/2231.

MLA Handbook (7th Edition):

Wolfe, Sarah Anne. “Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity.” 2017. Web. 27 Feb 2021.

Vancouver:

Wolfe SA. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2017. [cited 2021 Feb 27]. Available from: http://dx.doi.org/10.26153/tsw/2231.

Council of Science Editors:

Wolfe SA. Molecular mechanisms underlying alcohol use disorder and major depressive disorder comorbidity. [Doctoral Dissertation]. University of Texas – Austin; 2017. Available from: http://dx.doi.org/10.26153/tsw/2231

2. Sosanya, Natasha Marie. mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p.

Degree: PhD, Cell and Molecular Biology, 2014, University of Texas – Austin

 Little is known about how a neuron undergoes site-specific changes in intrinsic excitability in normal and diseased conditions. We provide evidence for a novel mechanism… (more)

Subjects/Keywords: mTOR; Kv1.1; miR-129; HuD; mRNA degradation; Temporal lobe epilepsy

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APA (6th Edition):

Sosanya, N. M. (2014). mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/46489

Chicago Manual of Style (16th Edition):

Sosanya, Natasha Marie. “mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p.” 2014. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/46489.

MLA Handbook (7th Edition):

Sosanya, Natasha Marie. “mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p.” 2014. Web. 27 Feb 2021.

Vancouver:

Sosanya NM. mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/46489.

Council of Science Editors:

Sosanya NM. mTOR dependent regulation of Kv1.1 in normal and disease states by the RNA binding factors, HuD and miR-129-5p. [Doctoral Dissertation]. University of Texas – Austin; 2014. Available from: http://hdl.handle.net/2152/46489


University of Texas – Austin

3. Workman, Emily Rush. Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid receptor B (GABABR): Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and [gamma]-aminobutyric acid receptor B (GABABR).

Degree: PhD, Neuroscience, 2016, University of Texas – Austin

 N-methyl-D-aspartate receptor (NMDAR) antagonists have gained much attention of late for their ability to remediate major depressive disorder. The body of evidence surrounding their mechanism… (more)

Subjects/Keywords: GABAB receptor; NMDA receptor; Homeostasis; Hippocampus; Rapid antidepressants; Depression; Cultured neurons

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APA (6th Edition):

Workman, E. R. (2016). Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid receptor B (GABABR): Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and [gamma]-aminobutyric acid receptor B (GABABR). (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/63884

Chicago Manual of Style (16th Edition):

Workman, Emily Rush. “Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid receptor B (GABABR): Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and [gamma]-aminobutyric acid receptor B (GABABR).” 2016. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/63884.

MLA Handbook (7th Edition):

Workman, Emily Rush. “Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid receptor B (GABABR): Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and [gamma]-aminobutyric acid receptor B (GABABR).” 2016. Web. 27 Feb 2021.

Vancouver:

Workman ER. Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid receptor B (GABABR): Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and [gamma]-aminobutyric acid receptor B (GABABR). [Internet] [Doctoral dissertation]. University of Texas – Austin; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/63884.

Council of Science Editors:

Workman ER. Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid receptor B (GABABR): Homeostatic interaction of N-methyl-D-aspartate receptor (NMDAR) and [gamma]-aminobutyric acid receptor B (GABABR). [Doctoral Dissertation]. University of Texas – Austin; 2016. Available from: http://hdl.handle.net/2152/63884


University of Texas – Austin

4. Chirillo, Michael August. Coordinated structural plasticity across synapses in the adult hippocampus.

Degree: PhD, Neuroscience, 2015, University of Texas – Austin

 Neural circuitry is determined primarily by trillions of synaptic junctions that link cells in the nervous system. Understanding how the structure of the synapse influences… (more)

Subjects/Keywords: Synaptic plasticity; Electron microscopy; Cell biology; Endoplasmic reticulum; Hippocampus; Structural plasticity; Neuroscience; Long-term potentiation

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APA (6th Edition):

Chirillo, M. A. (2015). Coordinated structural plasticity across synapses in the adult hippocampus. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/31594

Chicago Manual of Style (16th Edition):

Chirillo, Michael August. “Coordinated structural plasticity across synapses in the adult hippocampus.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/31594.

MLA Handbook (7th Edition):

Chirillo, Michael August. “Coordinated structural plasticity across synapses in the adult hippocampus.” 2015. Web. 27 Feb 2021.

Vancouver:

Chirillo MA. Coordinated structural plasticity across synapses in the adult hippocampus. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/31594.

Council of Science Editors:

Chirillo MA. Coordinated structural plasticity across synapses in the adult hippocampus. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/31594

5. Busch, David James. Deleterious effects of synuclein in injury-induced neurodegeneration and in a synaptic model of Parkinson’s Disease.

Degree: PhD, Cell and Molecular Biology, 2012, University of Texas – Austin

 Synucleins represent a conserved family of small proteins that include α-, β-, and γ- isoforms, which are highly expressed in neurons of the vertebrate nervous… (more)

Subjects/Keywords: Synuclein; Lamprey; Spinal cord injury; Reticulospinal neurons; Parkinson's Disease; Neurodegeneration; Neuronal death; Vesicle recycling; Synapse; Clathrin-mediated endocytosis

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

APA (6th Edition):

Busch, D. J. (2012). Deleterious effects of synuclein in injury-induced neurodegeneration and in a synaptic model of Parkinson’s Disease. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/ETD-UT-2012-08-6276

Chicago Manual of Style (16th Edition):

Busch, David James. “Deleterious effects of synuclein in injury-induced neurodegeneration and in a synaptic model of Parkinson’s Disease.” 2012. Doctoral Dissertation, University of Texas – Austin. Accessed February 27, 2021. http://hdl.handle.net/2152/ETD-UT-2012-08-6276.

MLA Handbook (7th Edition):

Busch, David James. “Deleterious effects of synuclein in injury-induced neurodegeneration and in a synaptic model of Parkinson’s Disease.” 2012. Web. 27 Feb 2021.

Vancouver:

Busch DJ. Deleterious effects of synuclein in injury-induced neurodegeneration and in a synaptic model of Parkinson’s Disease. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2012. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152/ETD-UT-2012-08-6276.

Council of Science Editors:

Busch DJ. Deleterious effects of synuclein in injury-induced neurodegeneration and in a synaptic model of Parkinson’s Disease. [Doctoral Dissertation]. University of Texas – Austin; 2012. Available from: http://hdl.handle.net/2152/ETD-UT-2012-08-6276

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