Oxidative Stress Alters IP3 Receptor Function in the Neuronal Cell Line HT22

Simple item page
dc.contributor.advisorPeter Koulen
dc.contributor.committeeMemberKati Prokai
dc.contributor.committeeMemberTina Machu
dc.creatorLongoria, Sandra
dc.date.accessioned2019-08-22T21:12:16Z
dc.date.available2019-08-22T21:12:16Z
dc.date.issued2008-05-01
dc.date.submitted2014-02-24T14:54:05-08:00
dc.description.abstractSandra Longoria., Oxidative Stress Alters IP3 Receptor Function in the Neuronal Cell Line HT22, Master of Science (Biomedical Sciences), May 2008, 72 pp., 25 Figures. 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 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 Ca2+ 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.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12503/29152
dc.language.isoen
dc.provenance.legacyDownloads0
dc.subjectCell and Developmental Biology
dc.subjectCell Biology
dc.subjectCells
dc.subjectCellular and Molecular Physiology
dc.subjectLife Sciences
dc.subjectMedical Cell Biology
dc.subjectMedicine and Health Sciences
dc.subjectMolecular and Cellular Neuroscience
dc.subjectNeuroscience and Neurobiology
dc.subjectNeurosciences
dc.subjectOther Cell and Developmental Biology
dc.subjectOxidative stress
dc.subjectIP3 Receptor Function
dc.subjectneuronal cell line HT22
dc.subjectAlzheimer’s Disease
dc.subjectneurodegenerative diseases
dc.subjectintracellular calcium channels
dc.subjectCa2+
dc.subjectneurons
dc.subjecttBHP
dc.subjecttert-butyl hydrogen peroxide
dc.titleOxidative Stress Alters IP3 Receptor Function in the Neuronal Cell Line HT22
dc.typeThesis
dc.type.materialtext
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameMaster of Science

Files

Original bundle

Now showing 1 - 1 of 1
Thumbnail Image
Name:
Longoria_OxidativeStressAltersIP3.pdf
Size:
17.94 MB
Format:
Adobe Portable Document Format
Download

Collections

School of Biomedical Sciences
Theses and Dissertations