Open Access Theses and Dissertations

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You searched for subject:(Rapid antidepressants). Showing records 1 – 2 of 2 total matches.

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University of Texas – Austin

1. 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

URL: http://hdl.handle.net/2152/63884 

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 of action suggests that they activate cellular homeostatic mechanisms. This thesis examines the convergence of rapid antidepressant and homeostatic mechanisms. It provides evidence of the homeostatic interaction between NMDAR and γ-aminobutyric acid receptor B (GABABR), a metabotropic inhibitory receptor, by demonstrating that GABABR function shifts from opening inwardly rectifying potassium channels to increasing resting dendritic calcium signal upon application of NMDAR antagonists. This fundamental shift in function plays an important role in the activation of protein synthesis dependent homeostatic mechanisms that occur in response to NMDAR antagonists. We hypothesize that the GABABR shift in function is a unifying pathway between rapid antidepressant and local homeostatic mechanisms. Advisors/Committee Members: Raab-Graham, Kimberly F. (advisor), Harris, Kristen (committee member), Johnston, Daniel (committee member), Sullivan, Christopher (committee member), Zemelman, Boris (committee member).

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

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

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

2. 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

URL: http://dx.doi.org/10.26153/tsw/2231 

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 of either disorder doubling the risk of developing the other. Despite their prevalence, few treatments are available to individuals with comorbid AUD and MDD. Both alcohol and antidepressants promote lasting neuroadaptive changes in synapses and dendrites. With alcohol these changes may provide relief from depressive symptoms, and the initial use of alcohol may be a form of self-medication for individuals with MDD, suggesting ethanol may have antidepressant properties underlying similarities in neurobiological abnormalities. However, the synaptic pathways that are shared by alcohol and antidepressants are unknown. This study aims to identify why acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviors. To understand the functional basis of these behaviors, a molecular pathway activated by rapid antidepressants was investigated. Here ethanol, like rapid antidepressants, altered γ-aminobutyric acid type B receptor (GABA [subscript B] R) expression and signaling, to increase dendritic calcium. New GABA [subscript B] Rs were synthesized in response to ethanol treatment, requiring fragile-X mental retardation protein (FMRP). Ethanol-dependent changes in GABA [subscript B] R expression, dendritic signaling, and antidepressant efficacy were absent in Fmr1-knockout (KO) mice. These findings indicate that FMRP is an important regulator of protein synthesis following acute alcohol exposure, and provided a molecular basis for the antidepressant efficacy of acute ethanol exposure. We identify alterations on a global scale with acute alcohol and antidepressant by sequencing the synaptic transcriptome. We identified parallel alterations in exon usage with acute alcohol and antidepressant treatment. These shared differentially expressed exons may give rise to isoforms and proteins with altered function or localization in the synapse. Some of these differentially expressed exons were identified in genes known to have alternative isoforms with AUD and MDD. These data implicate alternative splicing and isoform expression in the acute antidepressant-like effects of ethanol and the development of comorbid alcohol and depression. Understanding the molecular basis for comorbidity may aid in development of treatment options for afflicted individuals with dual disorders, as well as explore the mechanism for the initiation of addiction with acute exposure to alcohol Advisors/Committee Members: Harris, R. Adron (advisor), Raab-Graham, Kimberly F. (advisor), Golding, Nace (committee member), Morrisett, Richard (committee member), Macdonald, Paul (committee member).

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

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

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