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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
41

Mechanisms of dynorphin release and action in the hippocampus /

Simmons, Michele LeAnn. January 1996 (has links)
Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references.
42

Synaptic protein profiles and neurotransmitter release in relation to alcoholism /

Kuo, Sheng-Wen. January 2004 (has links) (PDF)
Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.
43

Regulation of the human dopamine transporter

Li, Libin. Reith, Maarten E. A. January 2002 (has links)
Thesis (Ph. D.)--Illinois State University, 2002. / Title from title page screen, viewed February 3, 2006. Dissertation Committee: Maarten E.A. Reith (chair), Hou Tak Cheung, Paul A. Garris, Stephen M. Lasley, Brian J. Wilkinson. Includes bibliographical references and abstract. Also available in print.
44

Studies of G-protein coupled receptors using pertussis toxin

Van der Ploeg, Ingeborg. January 1991 (has links)
Thesis (doctoral)--Karolinska Institutet, Stockholm, 1991. / Extra t.p. with thesis statement inserted. Includes bibliographical references.
45

Studies of G-protein coupled receptors using pertussis toxin

Van der Ploeg, Ingeborg. January 1991 (has links)
Thesis (doctoral)--Karolinska Institutet, Stockholm, 1991. / Extra t.p. with thesis statement inserted. Includes bibliographical references.
46

Development of the presynaptic nerve terminal during neuromuscular synaptogenesis /

Lee, Chi Wai. January 2005 (has links)
Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2005. / Includes bibliographical references (leaves 136-146). Also available in electronic version.
47

Glutamate antagonism as a potential treatment of Parkinson's Disease : a study in a rat model

Leung, Cheuk Hung 01 January 2007 (has links)
No description available.
48

Neurochemical Coding of Myenteric Neurons in the Guinea-Pig Antrum

Vanden Berghe, P., Coulie, B., Tack, J., Mawe, G. M., Schemann, M., Janssens, J. 17 July 1999 (has links)
Electrophysiological studies of myenteric neurons in the guinea-pig antrum suggest that different neuroactive compounds are involved in synaptic transmission. It is not known what neurotransmitters and neuropeptides are present and to what extent they colocalize. Immunohistochemical stainings were performed on whole-mount preparations of the guinea-pig antrum. Immunoreactivity for neuron-specific enolase was used as a general marker and was set at 100%. There was no overlap between cholinergic and nitrergic neurons, resulting in two separate subpopulations. The presence of choline acetyltransferase immunoreactivity was used to identify the cholinergic subset, which accounted for 56% of the cells. Immunoreactivity for nitric oxide synthase, on the other hand, was displayed in 40.7% of the neurons. Substance-P immunoreactivity was present in 37.4% of the cells and vasoactive intestinal peptide and neuropeptide Y in 21.7% and 28.6%, respectively. Small subsets of neurons had immunoreactivity for serotonin (3.9%), calretinin (6.8%) and calbindin (0.5%). Colocalization studies revealed several subgroups of neurons, containing one or more of the screened markers. Though some similarity is found in the chemical coding of the antrum compared to that of the small intestine and the corpus, remarkable differences can be seen in the occurrence of some subpopulations. Cholinergic neurons are not as predominant as in other parts of the gut, serotonin presence is doubled and some vasointestinal-peptide-positive neurons express substance P. These differences might reflect the highly specialized function of the antrum; however, the exact role of these classes remains to be established.
49

Hypoxia-Induced Cardiac Arrest Alters Central Nervous System Concentrations of the GLYT2 Glycine Transporter in Zebrafish (Danio rerio)

Auzenne, Alexis 07 1900 (has links)
Hypoxia as a stressor has physiological implications that have been a focal point for many physiological studies in recent years. In some studies, hypoxia had large effects on the organ tissue degeneration, which ultimately effects multiple ecological processes. These organ tissue studies played a part in the development of new fields like neurocardiology, a specialty that studied the relationship between the brain and the heart. This thesis focuses on how hypoxia-induced cardiac arrest alters the amounts of GLYT2, a glycine reuptake transporter, in the central nervous system of zebrafish, Danio rerio. At 7 days post-fertilization (dpf), zebrafish were exposed to acute, severe hypoxia until they lost equilibrium, and minutes later, subsequent cardiac arrest occurred. Zebrafish were then placed into recovery groups to measure the GLYT2 levels at multiple points in zebrafish recovery. Fish were then sacrificed, and their brains dissected. Using immunofluorescence, the outer left optic tectum of the zebrafish was imaged, and mean image pixel fluorescent intensity was taken. There were significant changes (one-way ANOVA) in the levels of GLYT2 compared to that of the control groups during the course of recovery. GLYT2 levels continued to rise through the 24-hour recovery mark but did not show significant difference after 3 hours of recovery. This suggest that GLYT2 levels increased rapidly in the first 3 hours of recovery and continued to increase through 24 hours at a slower rate. Changes in GLYT2 levels may affect motor and sensory information, movement, visualization, and audition in these zebrafish. Further research should be conducted to determine how long it takes for GLYT2 levels to return to baseline, as well as behavioral measurements through each recovery period as it relates to glycine function.
50

Astrocytic Transporters in Alzheimer’s disease

Ugbode, Christopher I., Yuhan, H., Whalley, B.J., Peers, C., Rattray, Marcus, Dallas, M. 29 November 2016 (has links)
Yes / Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer’s disease. These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease modifying therapies for Alzheimer’s disease, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic support, neurotransmission and synaptic architecture. Therefore, specific targeting of individual transporter families has the potential to suppress neurodegeneration, a characteristic hallmark of Alzheimer’s disease. A small number of the four hundred transporter superfamilies’ are expressed in astrocytes, with evidence highlighting a fraction of these are implicated in Alzheimer’s disease. Here we review the current evidence for six astrocytic transporter subfamilies involved in Alzheimer’s disease, as reported in both animal and human studies. This review confirms that astrocytes are indeed a viable target, highlights the complexities of studying astrocytes and provides future directives to exploit the potential of astrocytes in tackling Alzheimer’s disease. / BBSRC, Alzheimer's Society, Motor Neuron Disease Association

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