Created by Anna mph
about 9 years ago
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What are the diseases that are in which glutamate-induced neuronal death can be seen?
Define necrosis
Define apoptosis. What is it used for?
What are the characteristics of apotosis?
What can cause apoptosis to occur in healthy cells?
What do elevated levels of extracellular glutamate cause?
What are the three key elements in the cascade of cell death?
Why is increased influx of Na+ bad?
Why is increased Ca2+ influx bad?
Why is increased glutamate exocytosis bad?
What happens in slow excitotoxicity?
What are the two components excitotoxicity?
What are the two things that happen as a result of Ca2+ overload in a cell?
What are the three pathways through receptors which mediate excitotoxicity?
Starting from head injury etc. to Calcium overload.
1)
2/3)
What is oxidative stress?
What are the two different pathways that can cause oxidative stress?
What happens when mitochondria 'mop up' intracellular calcium?
Name a free radial
What effect does the ATP deficiency have on extracellular glutamate concentrations?
What effect to free radicals have on neurons and what else does superoxide do?
Which enzyme is responsible for destroying superoxide? Why doesn't it do so during oxidative stress?
What is thought to occur in Huntington's disease in terms of free radicals?
Which enzymes are activated by calcium influx?
What effect does the activation of PLA2 have?
What effect does the activation of nNOS have?
What does the NO" react with? What does this produce and what damage does this cause, how can it cause this damage?
What is activated in response to inflammation and what does this cause?
What damage do lipases, proteases and endonucleases cause?
What are the two causes of stroke?
What three major processes occur in an ischaemic stroke?
What is inflammation caused by? How does this effect extracellular glutamate levels?
What can be used to treat a patient within three hours of having a stroke? How does it work?
Why can't treatment with tPA be used for a prolonged duration?
Which type of stroke is treatment with a tPA limited to and what is required for diagnosis?
After blood supply has been restored after a stroke what can continue to cause damage?
How long do you have to give treatment and what is this called?
What does ischaemia create in terms of neurons and what is it surround by?
What effect should an ionotropic GluR antagonist or Glu release inhibitor have on neurons?
Why is there an anti-excitotoxic hypothesis?
What have been the problems with treatments that try to decrease the effect of increased glutamate?
What are the two underlying problems with targeting glutamatergic receptors?
What characterises ALS (amyotrophic lateral sclerosis), symptoms and histology.
When is ALS usually diagnosed and how long do people usually survive post diagnosis?
What happens in terms of glutamate levels? How does this happen? Which receptor type is effected and what does this lead to?
What is Riluzole?
What is domoic acid/domoate? Where is it found?
What happens in amnesic shellfish poisoning? Why?
What would expect to see in the hippocampus of an animal which ingested domoic acid?
What is the kindling response?
What effect to NMDAR antagonists have on seizures?
How do repeated seizures lead to excitotoxicity?
What is Rasmussen's enchephalitis?
What is PERAMPANEL?