L20 - Glia Flashcards

1
Q

Ependymal cells

A

CSF production

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2
Q

Satellite cells

A

Precursors to skeletal muscle cells

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3
Q

Name one specialised retina glial cell and its functions

A

Muller cells

PASSIVE function (repsond when neurons fire AP):

  • Uptake and recycling of NT
  • Siphoning of K+ to blood stream
  • Energy metabolism (take glucose from blood and send metabolites of glucose to neurons, keeping them alive)
  • Maintenance of the Blood retinal barrier

ACTIVE functions
-Control neural function

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4
Q

If glial cells glutamate transporters are inhibited - what happens to the cells?

A

They are more depol.

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5
Q

Is K+ found in high conc during depol or hyperpol?

A

Depol

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6
Q

How do Muller cells siphon K+?

A

Using inwardly rectifying K+ channels (eg. Kir2.1, 4.1) where muller cells are wrapped around every synapse and shunt K+ to blood vessels, vitreous etc

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7
Q

Are glia cells excitable?

A

Yes - they have modulations in intracell. Ca2+ that can be initiated by NT, trauma, inflammatory mediators and spontaneously

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8
Q

How do glia control neural function?

A

1) Release gliotransmitters that directly excite or inhibit neurons

E.g. Increase in intracell. Ca2+ leads to release of ATP which breaks down to adenosine which is inhibitory -> hyperpol. adjacent cells, in this case: GC

  • This is neuroprotective as damaged cells release ATP
    2) Vasculature regulation - astrocytes surround blood vessels where Ca2+ wave initiated within an astrocyte causes vasocon. or vasodil.

E.g. They sense metabolic needs of neurons as there are wrapped around the synapse and when it is more active, astrocytes contact the blood vessels to vasodilate and increase blood flow

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9
Q

What happens in disesase - when there is loss of glial cells?

A

Loss of NT uptake
-Causes excessive stimulation of neurons and ultimately death

Loss of K+ uptake
-Changes in water balance (retinal oedema)

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10
Q

Gliosis

A
  • Hypertrophy (increased size) and hyperplasia (increased number) of glial cells
  • Increase expression of intermediate filaments (e.g. GFAP - glial fibrilary acidic protein which indicates cells got bigger)
  • Functional changes where there is altered: K+ channel expression, NT uptake, energy metabolism and water balance
  • Occurs in virtually all CNS diesases
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11
Q

Microglia come from? x% in mouse retina and pain? Function?

A

Bone marrow (haemopoietic), 5-20%, To remove damaged cells (macrophage-like function)

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12
Q

How do microglia play a role in the development of NS? Modulate neural integrity?

A

By refining synapses e.g. Overlap of GC dendrites from each eye to thalams hence microglia refine it by phagocytosisng synapses that aren’t needed/active

Cone photoreceptors are modified by microglia where microglia make sure they can respond to light and that the cone opsin is in the right spot

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13
Q

What happens during loss of microglia?

A

Lack of microglia exacerbates neurodegen (e.g. ALS, AD, retinal degen)

Esp in AD where B-amyloid and complement 1 (C1 - which are found coating synapses) stimulates microglial engulfment of synapses

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14
Q

The quadpartite synapse

A

1) Pre synaptic terminal
2) Post synaptic terminal
3) Astrocyte - NT uptake and recycling, K+ siphoning, release of gliotransmitters (ATP)
4) Microglia - synaptic pruning, release of cytokines

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15
Q

Macroglia aka

A

Astrocytes and Muller cells

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