Citation
Sullivan, Brian M. (1998) Studies of Nitric Oxide Signal Transduction. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/q269-0e91. https://resolver.caltech.edu/CaltechTHESIS:07312025-023246266
Abstract
Nitric oxide (NO) is released by many cells of the body, acting both as a signaling molecule or as a cytotoxic agent. In order to further our understanding of the mechanisms by which NO may function in the nervous system to regulate synaptic function, the following topics have been studied: 1) The NO-stimulated ADP ribosylation of synaptosomal proteins. 2) The subcellular localization of the neuronal isoform of nitric oxide synthase (nNOS) when the enzyme was overexpressed in embryonic hippocampal neurons by gene transfer with a recombinant adenovirus. 3) The release of NO and its primary metabolite, nitrite, as assayed by an electrochemical NO meter, from cultured cells infected with recombinant adenovirus expressing either nNOS or eNOS. Furthermore, the effects of inhibiting membrane attachment of eNOS were examined. From these studies, in Chapter 4, we conclude that the known reaction rates of NO with O2 do not account for the observed large ratio of nitrite to NO.
Item Type: | Thesis (Dissertation (Ph.D.)) |
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Subject Keywords: | (Biology) |
Degree Grantor: | California Institute of Technology |
Division: | Biology |
Major Option: | Biology |
Thesis Availability: | Public (worldwide access) |
Research Advisor(s): |
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Thesis Committee: |
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Defense Date: | 1998 |
Record Number: | CaltechTHESIS:07312025-023246266 |
Persistent URL: | https://resolver.caltech.edu/CaltechTHESIS:07312025-023246266 |
DOI: | 10.7907/q269-0e91 |
Default Usage Policy: | No commercial reproduction, distribution, display or performance rights in this work are provided. |
ID Code: | 17576 |
Collection: | CaltechTHESIS |
Deposited By: | Ben Maggio |
Deposited On: | 31 Jul 2025 18:55 |
Last Modified: | 31 Jul 2025 19:36 |
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