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- Title
- Origin of glutamate release in the normoxic, anoxic and ischemic isolated turtle cerebellum (Trachemys scripta).
- Creator
- Thompson, John William., Florida Atlantic University, Lutz, Peter L.
- Abstract/Description
-
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...
Show moreThe 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.
Show less - Date Issued
- 2001
- PURL
- http://purl.flvc.org/fcla/dt/12803
- Subject Headings
- Trachemys scripta, Turtles, Cerebral anoxia
- Format
- Document (PDF)
- Title
- Role and Regulation of Methionine Sulfoxide Reductase (Msr) in a model of oxidative stress tolerance: Trachemys scripta.
- Creator
- Reiterer, Melissa, Milton, Sarah, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
- Abstract/Description
-
The detrimental effects of oxidative stress caused by the accumulation of Reactive Oxygen Species (ROS) have been acknowledged as major factors in aging, senescence and several neurodegenerative diseases and conditions such as Parkinson’s disease and stroke (ischemia/reperfusion). Mammalian models are extremely susceptible to these stresses that follow the restoration of oxygen after anoxia; however, some organisms including the freshwater turtle Trachemys scripta can withstand several bouts...
Show moreThe detrimental effects of oxidative stress caused by the accumulation of Reactive Oxygen Species (ROS) have been acknowledged as major factors in aging, senescence and several neurodegenerative diseases and conditions such as Parkinson’s disease and stroke (ischemia/reperfusion). Mammalian models are extremely susceptible to these stresses that follow the restoration of oxygen after anoxia; however, some organisms including the freshwater turtle Trachemys scripta can withstand several bouts of anoxia and repeated reoxygenation without any apparent pathology. T. scripta thus provides us with an alternate vertebrate model in which we can investigate physiological mechanisms of neuroprotection without the damaging effects that come with oxidative stress. The major objective of this study was to investigate the protective mechanisms in the turtle brain under conditions of anoxia and oxidative stress. Specifically, the focus is on the Methionine Sulfoxide Reductase system (Msr), an antioxidant and cellular repair system, and how it is regulated to protect the brain against such stressors. Previous studies in my lab have demonstrated that Msr mRNA and protein levels are differentially upregulated during anoxia and reoxygenation. To investigate the regulation of Msr, FOXO3a was directly induced by transfecting a human FOXO3a plasmid into turtle brain cell cultures, as FOXO3a has been shown to regulate MsrA levels in other animal models. Pharmacological manipulation of FOXO3a was also performed using the green tea extract Epigallocatechin gallate (EGCG) as it has been shown to increase expression of FOXO3a during oxidative stress conditions in other models. I found that an induction of human FOXO3a increased FOXO3a levels and showed protection against cell death during oxidative stress. Furthermore, treatment of cells with EGCG increased expression of FOXO3a only when the cells were exposed to oxidative stress and decreased cell death. Induction of FOXO3a and EGCG treatment did not increase MsrA levels, however MsrB3 levels were upregulated under both treatments but only in the presence of oxidative stress. These results suggest that MsrA and MsrB3 protect the cells from oxidative stress damage through different molecular pathways and that EGCG may be a therapeutic target to treat diseases related to damage by oxidative stress.
Show less - Date Issued
- 2018
- PURL
- http://purl.flvc.org/fau/fd/FA00013154
- Subject Headings
- Methionine Sulfoxide Reductases, Oxidative Stress, Trachemys scripta
- Format
- Document (PDF)