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You searched for subject:(Synaptoneurosomes). Showing records 1 – 3 of 3 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 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 April 13, 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. 13 Apr 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 Apr 13]. 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


University of Illinois – Urbana-Champaign

2. Maki, Agatha. Analyzing peptide release using mass spectrometry.

Degree: PhD, 0323, 2014, University of Illinois – Urbana-Champaign

Neuropeptides are cell-to-cell signaling molecules that act as neurotransmitters, neuromodulators and hormones that impact a large variety of neuronal processes. The term neuropeptide refers to bioactive peptides made in neuron, stored in vesicles, and released into the extracellular space. While many peptides can be detected in a tissue homogenate, these will include processing intermediates and even protein degradation products. It is of great interest in the field of peptidomics to focus on functional characterization of proteins products such as cell-to-cell signaling peptides that are released from specific neuronal tissues, whether a brain region or specific cell. A variety of analytical techniques have emerged over the years to analyze neuropeptide release, and these methods have enabled scientists to characterize thousands of brain peptides. The focus of this research was on using various sampling approaches coupled to matrix-assisted laser desorption/ionization-mass spectrometry (MALDI MS) to analyze neuropeptide release from rodent brains. Chapter 2 is a general overview of the current state of analytical methods used to characterize neuropeptide release from cells to animals. Chapter 3 highlights two methods demonstrating neuropeptide release in a mouse model of fragile X syndrome. Sampling techniques using synaptoneurosomes and ex vivo brain slices were used to show a neuropeptide release deficit in Fmr1 KO mice. Chapter 4 highlights an approach utilizing in vivo microdialysis coupled to offline MALDI MS. This method was used to characterize extracellular peptide release from the hippocampus of rats in response to saline or morphine injection coupled with a spontaneous alternation task. In particular, fibrinopeptide A, a peptide derived from the fibrinogen α-chain, was significantly upregulated in rats exposed to morphine and spontaneous alternation testing. The functional consequence of fibronopeptide A release is still under investigation. The advancement of such analytical approaches to characterize neuropeptide release from a variety of samples ranging from cells to animals enables new discovery efforts for understanding the physiological and behavioral role of unknown peptides. Advisors/Committee Members: Sweedler, Jonathan V. (advisor), Sweedler, Jonathan V. (Committee Chair), Gillette, Martha U. (committee member), Ceman, Stephanie S. (committee member), Galvez, Roberto (committee member).

Subjects/Keywords: Peptides; Neuropeptides; Peptide Release; Mass Spectrometry; Fragile X Syndrome; Synaptoneurosomes; Brain Slices; Rab3A; Dense-Core Vesicles; Morphine; In Vivo Microdialysis; Hippocampus; Fibrinogen; Fibrinogen-α Chain Peptides; Fibrinopeptide A.

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

APA (6th Edition):

Maki, A. (2014). Analyzing peptide release using mass spectrometry. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/49662

Chicago Manual of Style (16th Edition):

Maki, Agatha. “Analyzing peptide release using mass spectrometry.” 2014. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed April 13, 2021. http://hdl.handle.net/2142/49662.

MLA Handbook (7th Edition):

Maki, Agatha. “Analyzing peptide release using mass spectrometry.” 2014. Web. 13 Apr 2021.

Vancouver:

Maki A. Analyzing peptide release using mass spectrometry. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2014. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/2142/49662.

Council of Science Editors:

Maki A. Analyzing peptide release using mass spectrometry. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2014. Available from: http://hdl.handle.net/2142/49662


University of the Western Cape

3. Egunlusi, Ayodeji Olatunde. Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection .

Degree: 2014, University of the Western Cape

This study focused on the synthesis of a series of novel tricycloundecane derivatives and evaluation of these compounds for neuroprotection using the fluorescent ratiometric calcium assay that indicates the ability of the test compounds to inhibit NMDA receptors and VGCC. The cycloaddition reaction between p-benzoquinone and monomerised dicyclopentadiene yielded tricycloundeca- 4,9-diene-3,6-dione which was used as the base structure and further derivatised. These derivatives were conjugated with benzylamine to form a series of imines and amines. A total of 10 compounds were synthesised for evaluation of inhibition of calcium influx through NMDA receptor channels and voltage-gated calcium channels. The structures were confirmed using NMR, IR and MS. On the proton NMR, the characteristic AB-quartet system was observed in the region of 1-2 ppm for all the compounds and the aromatic moiety was observed between 6.5-7.5 ppm for the novel polycyclic amines. These, with other functional groups, were used to confirm the individual structures Advisors/Committee Members: Joubert, Jacques (advisor), Malan, Sarel (advisor).

Subjects/Keywords: Neurodegenerative disorders; Tricycloundecane; N-methyl-D-aspartate receptor; Voltage-gated calcium channel; Oxidative stress; Synaptoneurosomes; Excitotoxicity; Apoptosis; Necrosis; Polycyclic cage; Neuroprotective agents; Fura-2 AM

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

APA (6th Edition):

Egunlusi, A. O. (2014). Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/3904

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):

Egunlusi, Ayodeji Olatunde. “Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection .” 2014. Thesis, University of the Western Cape. Accessed April 13, 2021. http://hdl.handle.net/11394/3904.

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

MLA Handbook (7th Edition):

Egunlusi, Ayodeji Olatunde. “Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection .” 2014. Web. 13 Apr 2021.

Vancouver:

Egunlusi AO. Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection . [Internet] [Thesis]. University of the Western Cape; 2014. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/11394/3904.

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

Council of Science Editors:

Egunlusi AO. Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection . [Thesis]. University of the Western Cape; 2014. Available from: http://hdl.handle.net/11394/3904

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

.