Date of Award
2001
Document Type
Thesis
Publication Status
Version of Record
Submission Date
October 2026
Thesis/Dissertation Advisor [Chair]
Lutz, Peter L.
Abstract
The uncontrolled release of glutamate is thought to be a key event in the death of the anoxic/ischemic mammalian brain. However the origin of glutamate, vesicular and/or cytoplasmic, is unknown. Likewise, the anoxic turtle releases a surge of glutamate upon anoxic depolarization. Therefore, this study investigated the origin of glutamate release in the isolated cerebellum of the freshwater turtle (Trachemys scripta). The results showed that: during anoxia, low extracellular glutamate levels are maintained, an ability lost during in vitro ischemia, by a reduction in glutamate release. Upon anoxic depolarization glutamate release originates from the cytoplasm. The lack of vesicular glutamate release is likely the result of an inhibition of vesicular exocytosis. However during in vitro ischemia, the inhibitory signal which blocks vesicular glutamate release during anoxia is lost. This allows a biphasic pattern of glutamate release during ischemia originating initially from vesicular stores which then causes cytoplasmic glutamate release.
Extent
36 p.
Recommended Citation
Thompson, John William, "Origin of glutamate release in the normoxic, anoxic and ischemic isolated turtle cerebellum (Trachemys scripta)" (2001). Electronic Theses and Dissertations 2000 - 2009. 269.
https://digitalcommons.fau.edu/etd_general_5/269
Identifier
FADT12803
Comments
FAU Electronic Theses and Dissertations Collection|Thesis (M.S.)--Florida Atlantic University, 2001.|Charles E. Schmidt College of Science|FAU Electronic Theses and Dissertations Collection