Exam 20: The Nervous System and Exposure to Lipophilic Toxicants or Transported Neurotoxic Agents

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How might calcium disruption cause brain toxicity?

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Via NMDA receptor (e.g. glutamate) or non-NMDA receptor (domoic acid).

How is the choroid plexus of interest in determining damage to the BBB?

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This is the site of CSF which bathes the brain. Metal damage here is separated in direct damage (Hg & Cd), transthyretin production and secretion pathway (Pb), and sequestered protective metal portion (Fe, Ag, Au).

What are examples of chemicals that alter gene expression to cause at least part of their neurotoxicity?

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Glutamate (immediate-early gene), aglycemia (heat shock/stress protein genes), trimethyltin (stannin expression), ischemia (ubiquitin expression), and methylmercury chloride (developmental gene expression). Other agents that may affect gene expression via oxidative stress (paraquat), mitochondrial disruption (NH3), slow-developing
neurodegeneration (Al), and prolonged CNS depression (solvent exposures).

What is the blood-brain barrier and how is it breached by agents such as 3-chloropropanediol?

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How can protein disruption lead to CNS problems?

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