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Involvement of protein kinase C in the evoked release of glutamate / by Debbie A. Zetts Dalrymple.

Author/creator Dalrymple, Debbie A. Zetts author.
Other author/creatorTerrian, David M., degree supervisor.
Other author/creatorEast Carolina University. Department of Biology.
Format Theses and dissertations and Archival & Manuscript Material
Production Info 1994.
Descriptionxvi, 134 leaves, 8 unnumbered leaves of plates : illustrations (some color) ; 28 cm
Supplemental Content Access via ScholarShip
Subject(s)
Summary Neurotransmitter release occurs when depolarization of the membrane of presynaptic nerve terminals opens voltage-sensitive calcium channels, and allows calcium influx and diffusion into the cell. The rise in intracellular calcium binds intracellular receptor proteins that mediate the fusion of synaptic vesicles with the presynaptic plasma membrane resulting in the release of vesicle contents (quanta) to postsynaptic receptors. There are many stages involved that prepare a nerve terminal that is at rest (polarized plasma membrane) for exocytosis and subsequent reactivation in response to subsequent action potentials. In order for neurons to respond to constant or repeated stimuli, neurons have networked many regulatory pathways to modulate signal transduction and synaptic vesicle recycling. Surface receptors are coupled to cytosolic regulatory molecules through four major second messenger pathways mediated by cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), calcium and the hydrolysis products of phosphatidylinositol. These second messengers catalyze the transfer of the r-phosphate from ATP to proteins that cause a conformational change which can regulate their function. Much attention has been focused on protein kinase C (PKC) as a possible mechanism in the phosphorylation of signal transduction cascades to facilitate glutamate exocytosis. This study attempts to elucidate the effect PKC activation has on the cascade of events modulating exocytosis. Specifically, examining the activation of PKC through the use of phorbol esters and its effects on K'^-evoked release of glutamate from hippocampal mossy fiber synaptosomes.
General noteSubmitted to the faculty of the Department of Biology.
General noteAdvisor: David M. Terrian
Dissertation noteM.S. East Carolina University 1994
Bibliography noteIncludes bibliographical references (leaves 124-134).
Genre/formAcademic theses.
Genre/formAcademic theses.
Genre/formThèses et écrits académiques.

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