Vascular and Metabolic Changes in Epilepsy and the Effects of Vascular Endothelial Growth Factor
Item
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Title
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Vascular and Metabolic Changes in Epilepsy and the Effects of Vascular Endothelial Growth Factor
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Identifier
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d_2009_2013:fb625be1b531:11565
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identifier
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12080
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Creator
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Scorpio, Kerri A.,
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Contributor
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Susan D. Croll
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Date
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2012
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Language
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English
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Publisher
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City University of New York.
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Subject
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Physiological psychology | Neurosciences | Epilepsy | Metabolism | Vasculature | VEGF
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Abstract
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Preliminary research has shown possible vascular morphological changes in the hippocampus of adult rats and humans after seizure activity. Research has shown high blood vessel density associated with high seizure frequency (Rigau et al., 2007) and vessel diameter enlargement has been observed with SE. We expected long term vascular morphological changes present in the hippocampus in rats after status epilepticus to be similar to the vascular morphological changes present in humans with temporal lobe epilepsy. We found a greater mean density of blood vessels in the rat hippocampus after SE. In human temporal lobe epilepsy tissue we found a greater mean density of blood vessels in the CA3 region of the hippocampus.;Research has shown that one day after SE, VEGF protein protects neurons from damage (Croll et al., 2004a; Nicoletti et al., 2008). We were interested in whether VEGF might also drive changes in post-seizure vascular parameters. We predicted that VEGF treatment would lead to less dense blood vessels after SE, closer to that of controls. As predicted, we found less dense blood vessels after SE with VEGF. This could be a mechanism of VEGF's neuroprotection.;During SE there may be an increased need by neurons for oxygen and glucose and this can result in increased metabolic load and increased vasculature. One potential component of VEGF's neuroprotective actions could be its role in decreasing electrical or metabolic activity during or after seizures. When applied to hippocampal slices, VEGF significantly decreases circuit excitability (McCloskey et al., 2005). VEGF may decrease metabolic activity via glucose transporters. We measured Glut-1 and Glut-4 expression after SE and found less Glut-1 and Glut-4 expression with VEGF. This change could be a mechanism of VEGF's neuroprotection by decreasing metabolic load and vascular need.;To explore if the transporter expression was functional the amount of glucose uptake in the hippocampus was measured. A study by Sheth et al., (2009) showed glucose uptake is significantly increased in the brain of an animal with seizures compared to controls. Our results were consistent in showing greater glucose uptake in the hippocampus after SE and VEGF may reduce glucose uptake.
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Type
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dissertation
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Source
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2009_2013.csv
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degree
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Ph.D.
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Program
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Psychology
