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Oxidative stress alters IP(3) recept...

University of North Texas Health Science Center at Fort Worth.

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Oxidative stress alters IP(3) receptor function in the neuronal cell line HT22.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Oxidative stress alters IP(3) receptor function in the neuronal cell line HT22./
Author:	Longoria, Sandra.
Description:	73 p.
Notes:	Source: Masters Abstracts International, Volume: 47-04, page: 2170.
Contained By:	Masters Abstracts International47-04.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=1462953
ISBN:	9781109019414

Oxidative stress alters IP(3) receptor function in the neuronal cell line HT22.
Longoria, Sandra.

Oxidative stress alters IP(3) receptor function in the neuronal cell line HT22. - 73 p.

Source: Masters Abstracts International, Volume: 47-04, page: 2170.

Thesis (M.S.)--University of North Texas Health Science Center at Fort Worth, 2008.

Oxidative stress contributes to the genesis of several neurodegenerative disorders such as Alzheimer's Disease (AD). Oxidants such as, tert-butyl hydrogen peroxide (tBHP), have been used in in vitro models of neurons and of neurodegeneration to induce oxidative stress. Small changes in the regulation of the intracellular calcium (Ca2+) concentration can contribute to brain aging and increase vulnerability of neurons to cellular and functional damage in neurodegenerative diseases. In neurons, inositol 1, 4, 5-trisphosphate (IP3), is a second messenger that is generated through receptor activity at the plasma membrane. IP3 receptors (IP3R) are located on endoplasmic reticulum (ER) membranes and are intracellular calcium channels (ICC) that release Ca2+ into the cytoplasm in response to activation by their ligand IP3. The goal of the present study was to measure the contribution of ICCs to Ca 2+ dysregulation in neurons experiencing oxidative stress. I tested the hypothesis that oxidative stress induced with tBHP causes increased intracellular Ca2+ release via activation of IP3 receptors. I used the murine hippocampal cell line HT22, as a model for neuronal oxidative stress. Immunocytochemistry and Ca2+ imaging experiments were performed to identify areas of altered IP3R expression and activity under normal conditions and induced oxidative stress. tBHP treatment increased expression and Ca2+ release activity of neuronal IP3 receptors. My findings support that oxidative stress as seen in a number of neurodegenerative diseases negatively affects regulation of Ca2+ release through increased expression and activity of IP3 receptors.

ISBN: 9781109019414Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Oxidative stress alters IP(3) receptor function in the neuronal cell line HT22.
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020 $a 9781109019414
035 $a (UMI)AAI1462953
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100 1 $a Longoria, Sandra. $3 1023927
245 1 0 $a Oxidative stress alters IP(3) receptor function in the neuronal cell line HT22.
300 $a 73 p.
500 $a Source: Masters Abstracts International, Volume: 47-04, page: 2170.
502 $a Thesis (M.S.)--University of North Texas Health Science Center at Fort Worth, 2008.
520 $a Oxidative stress contributes to the genesis of several neurodegenerative disorders such as Alzheimer's Disease (AD). Oxidants such as, tert-butyl hydrogen peroxide (tBHP), have been used in in vitro models of neurons and of neurodegeneration to induce oxidative stress. Small changes in the regulation of the intracellular calcium (Ca2+) concentration can contribute to brain aging and increase vulnerability of neurons to cellular and functional damage in neurodegenerative diseases. In neurons, inositol 1, 4, 5-trisphosphate (IP3), is a second messenger that is generated through receptor activity at the plasma membrane. IP3 receptors (IP3R) are located on endoplasmic reticulum (ER) membranes and are intracellular calcium channels (ICC) that release Ca2+ into the cytoplasm in response to activation by their ligand IP3. The goal of the present study was to measure the contribution of ICCs to Ca 2+ dysregulation in neurons experiencing oxidative stress. I tested the hypothesis that oxidative stress induced with tBHP causes increased intracellular Ca2+ release via activation of IP3 receptors. I used the murine hippocampal cell line HT22, as a model for neuronal oxidative stress. Immunocytochemistry and Ca2+ imaging experiments were performed to identify areas of altered IP3R expression and activity under normal conditions and induced oxidative stress. tBHP treatment increased expression and Ca2+ release activity of neuronal IP3 receptors. My findings support that oxidative stress as seen in a number of neurodegenerative diseases negatively affects regulation of Ca2+ release through increased expression and activity of IP3 receptors.
590 $a School code: 1250.
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
710 2 $a University of North Texas Health Science Center at Fort Worth. $3 1021741
773 0 $t Masters Abstracts International $g 47-04.
790 $a 1250
791 $a M.S.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=1462953