University:
McMaster University
Course:
BIOLOGY 4T03 | Molecular and Cellular Neuroscience
Academic year:

2021
Views:

480

Pages:

1
Author:

Sabrina S.

Chapter 4 exam 2 content [13/12/2014] motor disorders Spinal cord lower motor unit injury Hyperkinesia genetic defect 80% glycine receptors not functioning 20% normal behavior symptom: exaggerated startle response No treatment Basal Ganglia Spongiform Encephalopathy -> "spongy brain disease" -> drastic loss of neurons Scrapie: sheep disease kuru: eating CNS tissue (canabolism) -> start in Da pathway in baser ganglia -> dose agent (depends the dose) CJD: creutzfeldt Jacob disease (blindness, hallucination, resting tremor) genetic in ages ↑ 55 "mad cow": bovine spongiform encephalopathy: 1982 chronic wasting disease: white tall deer what is the cause for spongiform encephalopathy? normal abnormal disease protein binding with a normal protein abnormal (shape) one theory conversion not duplication. How can a prion kill a neuron? Resistant to temperature ткихоть сам прair the plasma membrane on the soma. PRP normal ana prion prp How wowa you test to see if a prion is the causing agent? Lo 1 cow subject [normal], I cow subject fed prion ingested fro Human variability why can only some people ger CJD? gene susceptibility to prion diseases