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Origin of glutamate release in the normoxic, anoxic and ischemic isolated turtle cerebellum (Trachemys scripta)

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Date Issued:
2001
Summary:
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.
Title: Origin of glutamate release in the normoxic, anoxic and ischemic isolated turtle cerebellum (Trachemys scripta).
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Name(s): Thompson, John William.
Florida Atlantic University, Degree grantor
Lutz, Peter L., Thesis advisor
Type of Resource: text
Genre: Electronic Thesis Or Dissertation
Issuance: monographic
Date Issued: 2001
Publisher: Florida Atlantic University
Place of Publication: Boca Raton, Fla.
Physical Form: application/pdf
Extent: 36 p.
Language(s): English
Summary: 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.
Identifier: 9780493238791 (isbn), 12803 (digitool), FADT12803 (IID), fau:9678 (fedora)
Collection: FAU Electronic Theses and Dissertations Collection
Note(s): Thesis (M.S.)--Florida Atlantic University, 2001.
Charles E. Schmidt College of Science
Subject(s): Trachemys scripta
Turtles
Cerebral anoxia
Held by: Florida Atlantic University Libraries
Persistent Link to This Record: http://purl.flvc.org/fcla/dt/12803
Sublocation: Digital Library
Use and Reproduction: Copyright © is held by the author with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Use and Reproduction: http://rightsstatements.org/vocab/InC/1.0/
Host Institution: FAU
Is Part of Series: Florida Atlantic University Digital Library Collections.