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26 Cards in this Set
- Front
- Back
- 3rd side (hint)
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note
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Which glial cell has no cytoplasm on H-E stain?
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Microglia
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Where is each type of glial cell derived from (embryo)?
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Astrocyte/oligo=neuroectoderm
Microglia= bone marrow |
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Ratio of glia: neurons in CNS
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10 to 1
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Are glia produced/repaired during life?
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Yes
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Can neurons survive without glia and vice versa?
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NO
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What is the difference in terms of regenerating axons in PNS vs CNS?
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CNS: little long distance axon regrowth possible (ie cant regen after spinal transection)
PNS: potential for long distance axon regrowth after axonal transection |
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CNS fast neurotransmitters
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GABA=inhibitory
Glutamate=excitatory |
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GFAP staining shows what?
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Cytokeleton of astrocytes
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Physical support function of astrocytes?
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end feet on the endothelial cells (this is not BBB)= physical scaffold
little connective tissue (collagen in brain) |
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Metabolic function of astrocytes?
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astrocytic end feet carpet neuronal surfaces--> regulate extracellular ion concs and transfer of metabolites
end feet around synaptic terminals--> 1) Support synapse formation and isolate synapses 2) rapidly reuptake GABA and glutamate |
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Myelin proteins in CNS vs PNS?
* produced by oligo in CNS, Schwann in PNS |
proteolipid protein (MYELIN PROTEIN)=CNS
P0=PNS |
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Myelination differences in CNS vs.PNS?
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CNS= oligodendrocytes --> one oligodendrocytes to many axons and many myelin segments
PNS= schwann cells--> 1:1 ratio |
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Myelination function?
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Axonal integrity: axon will die without it
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Microglia function? and marker
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Response to injury
Immune surveillance (become macs) Cytokine production * can only seetheir nuclei; marker=CD68 |
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VEGETABLE method for identifying glia in CNS
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Potato= astrocyte
Tomato=oligo cell body Hot pepper= microglia |
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ISCHEMIC STROKE
Difference btwn center and periphery of ischemic injury area in terms of cellular reactions? |
Center= hypoxic-ischemic injury (neurons dying)
Periphery= non-lethal (adaptive) and reactive responses |
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What are the signs of hypoxic-ischemic injury in the center of ischemic stroke?(18-24 hours)
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Neuronal necrosis: ATP depletion, NA/K pump failure
Signs= karyolysis, cytoplasm shrinks, eosinophilia (red cell), cytotoxic edema(cell processes swell) |
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What are the signs of adaptive response in the periphery of ischemic stroke?
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Neurons: repair mechanisms activate (chromatolysis, abnormal accumulations)
Astrocytes: gliosis (pink swelling of cytoplasm) Microglia: become macrophages (bigger than normal) Oligos: loss of myelin(white/empty spaces on H/E) |
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What is the biochem underlying neuronal inj in ischemic stroke?
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ATP depletion
Mitochondr injury Changed membr perm --> Na/K pump messed up Influx of Ca2+ Degrade intracell prots GLUTAMATE EXCITAOTOX |
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Basis of GLUTAMATE EXCITATOX?
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CNS injury releases glutamate --> NMDA channels open --> influx of Ca and Na --> activation of intracellular enzymes (endonucleasis, PKC, digestives)
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Why are neurons most susceptible to necrosis in ischemic stroke?
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Neuronal necrosis= ATP depletion
Neurons= very high energy demands |
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Reactions of astrocytes in ischemic stroke?
Where are these changes seen? and When? |
REACTIVE GLIOSIS (nonspecific to infarct)
enlarged nucleus (HYPERTROPHY) increased RER Lots of GFAP bext seen at subacute infarct edge(1-2 wks) |
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Reactions of microglia in ischemic stroke?
Where are these changes seen? and When? |
- Microglia increase in number and size
- Increase phagocytotic activity --> become macrophages or cluster together - Lipid rich - bext seen at subacute infarct edge(1-2 wks) |
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Reactions of oligos in ischemic stroke?
Where are these changes seen? and When? |
- SECONDARY DEMYELINATION
- Decreased myelin staining (big white holes) - maybe fewer tomatoes - best seen at oldinfarct (months to years) |
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Would you see neurons showing adaptive reactions to injury in ischemic stroke?
What would you see as adaptive rxn of neurons? |
No --> highly susceptible to necrosis
ex of adaptive neuronal rxn: Atrophy (ALS, Alzheimer), accumulation of abnormal substances (neurofibr tangles, Lewy bodies), axonal degen (transection), central chromatolysis |
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