Effect of maternal separation on stress-related proteins measured in a 6-hydroxydopamine rat model of Parkinson’s disease

Master Thesis

2014

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University of Cape Town

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The developing central nervous system is especially vulnerable and research has implicated early life stress (ELS) as a potentiating factor to cell death in a rat model of Parkinson’s disease (PD). PD is a movement disorder resulting from the selective degeneration of dopamine neurons in the substantia nigra pars compacta (SNc). Dopamine neurons have been shown to exhibit mitochondrial dysfunction, oxidative stress and misfolded protein aggregation in patients with PD. Since ELS has been shown to negatively affect the nigrostriatal pathway and mitochondrial function, developmental stress may create a vulnerable microenvironment which results in a greater rate of cell death during the development of PD. Many proteins play a role in establishing a positive microenvironment that is neuroprotective, and may be good candidates for the mechanism by which ELS potentiates neurodegeneration in the PD rat model. This study aimed to investigate whether the finding that ELS increases neuronal susceptibility to 6-hydroxydopamine(6-OHDA)-induced degeneration of dopamine neurons occurs through dysregulation of the oxidative stress-related heat shock protein (HSP)25, or plasticity-related proteins, chondroitin sulphate proteoglycans (CSPGs) or Nogo-A.
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