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dc.contributor.supervisorWang, Jun-Feng (Pharmacology & Therapeutics)en_US
dc.contributor.authorWang, Ying
dc.date.accessioned2015-03-27T19:32:54Z
dc.date.available2015-03-27T19:32:54Z
dc.date.issued2015-03-27
dc.identifier.urihttp://hdl.handle.net/1993/30316
dc.description.abstractOxidative stress is one of the major characteristics in Alzheimer’s disease, and converging evidence indicates that cysteine S-nitrosylation might be related in AD pathology. My results demonstrated exogenous S-nitrosoglutathione was able to S-nitrosylate vAChT, vMAT2, vGluT1 and vGluT2. S-nitrosylation of these vesicular transporters inhibited the uptake of [3H]acetylcholine, [3H]dopamine and [3H]glutamate respectively. APP/PS1 transgenic mice were used to investigate neurotransmission dysfunctions of Alzheimer’s disease. Global protein S-nitrosylation was increased in the 9 and 12 month APP/PS1 mice. Further investigation demonstrated an increase of vAChT and vGluT1 S-nitrosylation in frontal cortex of 6, 9 and 12 month APP/PS1 mice and an increased vAChT and vGluT1 S-nitrosylation was found in hippocampus of 3 month APP/PS1 mice. These findings together suggest that S-nitrosylation of vesicular transporters inhibits the uptake of neurotransmitters, and S-nitrosylation of vAChT and might be associated with the neurotransmission dysfunction of acetylcholine and glutamate in Alzheimer’s disease.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectS-nitrosylationen_US
dc.subjectvesicular transporteren_US
dc.subjectnitric oxideen_US
dc.subjectAlzheimer's diseaseen_US
dc.titleOxidative modification of vesicular transporters in an animal model of Alzheimer’s diseaseen_US
dc.typeinfo:eu-repo/semantics/masterThesis
dc.typemaster thesisen_US
dc.degree.disciplinePharmacology and Therapeuticsen_US
dc.contributor.examiningcommitteeParkinson, Fiona (Pharmacology & Therapeutics) Eftekharpour, Eftekhar (Physiology & Pathophysiology)en_US
dc.degree.levelMaster of Science (M.Sc.)en_US
dc.description.noteMay 2015en_US


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