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Medneuro- neurophysiology (M1-2) > Glia > Flashcards

Glia Flashcards

1
Q

the two cell types in the brain

A

neurons and glial cells

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2
Q

who introduced the concept of Neuroglia?

A

Virchow (1856)

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3
Q

radial glial cells in the retina

A

Miller cells

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4
Q

radial glial cells in the cerebellum, and what type of glial cells are they considered?

A

Bergmann cells (astrocytes)

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5
Q

The three main types of glia cells and their general function

A
  1. Astrocytes- multifunctional cells, surround neurones and regulate the extracell. activity, neuronal activity, communication, energy supply, neuronal guidance.
  2. oligodendrocytes- myelination of axons in the CNS (and in the PNS Schwann cells have the same functions)
  3. Microglia- the “immune cells” of the brain, activated when brain damage occurs.
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6
Q

heterogeneity of glia cells (astrocytes, olig., microglia)

A

Astroglia- the most diverse glia in the CNS, no uniform shape, definition or function)

Oligodendrocytes- quite homogenous, mild differences in length of processes (spinal cord-longer bodies of oligode.)

Microglia- quite homogenous, but the exist in 2 forms- ramified, inactivated form, and amboid, activated form)

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7
Q

main types of intermediate filaments in astrocytes

A

GFAP, Vimentin

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8
Q

1 way to identify astrocytes

A

using GFAP as a specific marker for astroglia (although level of expression varies between different astroglia)

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9
Q

types of astrocytes and their function/location

A
  1. protoplasmic astrocytes
  2. fibrous astrocytes
  3. radial glia
  4. valate astrocytes
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10
Q

protoplasmic astrocytes

A

found in grey matter, have many fine processes; form perivascular endfeet, as well as connections w. neurons

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11
Q

fibrous astrocytes

A

found in white matter, have long robust processes, form perivasc./subpial and feet, and send perinodal processes to contact axons ar node of Ranvier.

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12
Q

radial glia

A

bipolar & ovoid body w. elongated processes; common feature of developing brain (first cells to develop from neuronal progenitors); they form a scaffold that helps in neuronal migration; after migration, most of them turn into astrocytes apart from in cerebellum and in the retina.

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13
Q

valate astrocytes

A

radial like cells; found in cerebellum, enwrap granular neurons; similar type found in neocortex (mainly in olfactory bulb); act as stem cells and can differentiate into other cell types later (glia or neurons)

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14
Q

radial glia after maturation

A

After maturation, radial glia “disappear” from most brain regions, apart from the retina (Müller cells) and cerebellum (Bergemann cells). the rest of them transform to stellate astrocytes.

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15
Q

Müller cells

A

located in the retina;
they make extensive contacts w. retinal neurons;
morphology- extending, longitudinal processes along rods and cones. each Müller cell forms contact w. a group of neurons organised in a columnar fashion.

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16
Q

Bergmann cells

A

located in the cerebellum;
morphology- relatively small cell body, w. 3-6 processes that extend from Purkinje cell layer to dial surface. At the start of development they are real radial cells but they change their morphology later on.
they surround Purkinje cell-dendrites and form contacts w. synapses.

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17
Q

Functions of astrocytes

A
  1. serve as stem cells
  2. define the brain microarchitecture (process= tiling)
  3. control extracellular k+ homeostasis (via spatial buffering or k+/na+ pump)
  4. removal of excess glutamate
  5. glutamine supply to maintain glutamatergic neurotransmission
  6. control blood flow and provide neurons w. metabolic substances
  7. control synaptogenesis and synaptic maintenance
  8. signalling- part of the triptate synapse
  9. singling of glia cells/glial activation and excitability (via ATP)
  10. substance release/global control
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18
Q

the triptate synapse

A

the triptate synapse- synapses are built from 3 equally important parts: presynaptic terminal, postsynaptic neuronal membrane and the surrounding glia.
astrocytes in grey matter are closely associated w. neuronal membranes and their synaptic regions.
- the close proximity allows astroglia to be exposed to NT release (–> close morphology and functionality)
- receptors on astroglia match the NT released by the synapse they cover.

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19
Q

process in triptate synapse

A

NT released from presynaptic terminal–> receptor activation in postsynaptic neuron & perisynaptic astrocyte–> generation of postsyn. potential and ca2+ signal in astroglia–>a. propagation through astrocyte; b. trigger release of NT from astrocyte–> signal onto pre-&postsynaptic neuron.

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20
Q

how do astroglia control extracell. k+ homeostasis?

A

a. spatial buffering (passive)- k+ is taken up at the site of high concentration and redistributed by astrocytes at sites where it’s low.
b. active process- increase in pump activity (e.g. na+/k+ ATPase)–> increasing intercell. k+ and water.

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21
Q

how do astrocytes remove excess glutamate, and maintain glutamate neurotransmission?

A

when glutamateis released in excess and for a long time it becomes neurotoxin. Astrocytes posses special glutamate co-transporters (energy supplied from na+ grad.) –> convert glutamate into glutamine–glutamine transported back to the neuron and converted back into glutamate.

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22
Q

Tiling

A
  • Astrocytes define the microarchitecture of the parenchyma by dividing the gray matter (tiling) and form relatively independent structural units.
  • Protoplasmic astrocytes create micro-anatomical domains (within their processes)–> membrane of astrocytes covers neuronal membrane and synapses and also send processes to neighbouring blood vessels and create neurovascular units (Neuron-astrocyte-blood vessel)
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23
Q

Radial glia as stem cells

A

neuroepithelial cells transform into radial glia–> recognised as neural precursor cell–> asymmetric division produces neuronal precursors–> migration of neurons to their destination (using radial glia as a scaffolding);
symmetric division of radial glia produces astrocytes and oligodendrocytes.

24
Q

in the extracell. space, astroglia control:

a. k+
b. glutamate
c. Na+
d. water
e. a, b & d

A

e

25
Q

glial cells are present in

a. the entire CNS and PNS
b. only in CNS
c. only in PNS
d. only in white matter
e. only in grey matter

A

a

26
Q

the major function of oligodendrocytes

A

myelin production

27
Q

myelin in the PNS is produced by

A

Schwann cells

28
Q

ways increase the speed of nerve conduction, which one is better? why?

A

a. myelin formation
b. increase of the axon diameter (e.g. squid)
the giant axon of the squid can reach similar velocities to myelinated motorneurons. but the myelin is a better strategy, as it reaches high speed and saves space (room in the skull is limited)

29
Q

all oligodendrocytes produce myelin-

true/false

A

False. some oligodend. are not directly connected to the myelin sheath (satellite oligodend. found in the grey matter, unknown function)

30
Q

the points, at which axons are not myelinated

A

nodes of Ranvier

31
Q

Schwann cells can myelinate the same amount of axons as oligodendrocytes (true/false)

A

False. each oligodendrocyte can myelinate up to 20 axons, whereas each Schwann cell is associated with 1 axon.

32
Q

proteins involved in myelin production. Are they the same in both CNS and PNS?

A

in CNS- MAG, MBP, PLP/DM20, PMP22
in pNS- MBP, PO, PMP22
–> Myelin is composed by a different set of proteins in PNS and CNS.

33
Q

myelin formation in rodents vs. humans (start/end?)

A

myelin formation in rodents starts at birth and is competed around 2 months PN.
in humans- 2nd half of fetal life, peak activity is 1 year PN and ends around 20 years PN

34
Q

myelin thickness is determined by

A

NR1

35
Q

Development of oligodendrocytes in brain, spinal cord, optic nerve

A

brain- precursors located in subventricular zone
spinal cord- ventral regions of the neural tube
optic nerve- 3rd ventricle

36
Q

proliferation of oligodend. progenitors is controlled by

A

growth factors released from neurons and astrocytes (PDGF, FGF). intrinsic mechanisms and environment control the proper amount required for myelination.
excess oligodend. are eliminated by apoptosis.

37
Q

linage of oligodendrocytes

A

Olig2+

  • > multiple progenitor cells
  • > specified cells
  • > NG2 cells *
  • > terminally differentiated oligodendrocytes
  • NG2 cells are antibodies that label progenitor cells.
38
Q

Development of Schwann cells (SC)

A

during development, SC are derived from undifferentiated neural crest cells–> immature SC produce either myelinating or non myelinating SC.

39
Q

morphology od Schwann cells

A

similar to oligodendrocytes, but with much smaller membrane (since they only myelinate 1 axon)

40
Q

myelin sheath - compartments ans structure

A

myelin sheath is form by enwrapment of axon by oligodend. or SC processes.

  • intercellular compartment (major dense)- very compressed, appears as a single line in EM.
  • double interperiod line- the outer surface of the lipid bylayer appears as a thick Lin separated by extracell. space.
  • -> this composition makes myelin poorly hydrated (70 % lipids, 30% proteins)
41
Q

How is the thickness of myelin is determined by NR1?

A

Axons send signal (NR1) to oligodend. –> NR1 binds to ERbB receptors in SC which define the ratio between axon diameter : axon diameter + myelin (g ratio)

42
Q

how does myelin enable saltatory nerve conduction?

A

axons are myelinated in bulks and myelin sheath is interrupted by the node of Ranvier, at which axons aren’t myelinated.
node of Ranvier is packed with na+ channels.
–> allows the saltatory (“jump”) conduction, since AP is only generated at node and so it spreads passively and rapidly through the myelinated parts to the next node.

43
Q

advantages of node of Ranvier

A
  • faster conduction

- energy efficient (since na+ accumulated only at the node)

44
Q

myelin modulation- parameters

A

certain tasks can trigger or modulate myelination–> some oligodend. start to proliferate and replace the existing ones (demyelination)
–> myelin is adjusting to reconstruction of connections and plasticity of connection (plasticity exists also at the connection level)

45
Q

relapse of disease in MS patients

A

oligodendrocytes proliferate regularly and replace existing ones in order to remyelinate axons. In MS there is degeneration of myelin. remyelination exists and patients get better in early stages but the degenration is too rapid in comparison to remyelination rate so patients “relapse” and decline

46
Q

microglia derive from progenitors that come from:

a. ectoderm
b. mesoderm
c. neuroepithelium

A

b.

47
Q

Microglia exist in 2 forms. what are their characteristics? in what circumstances do they appear?

A
  1. Ramified (resting) form- under physiological conditions MG exist in resting form. they have small cell body, thin processes which send multiple branches and extend in all directions.
    each MG has its own territory (15-30um), in which it constantly moving, scanning the environment looking for damages–> very rapid movement, the fastest moving structures in the brain).
  2. Ameoboid form- neuronal damage–> rapid movement of many MG processes towards the Sita of the lesion–> astrocyte signal MG by releasing ATP through gap junctions –> full activation of MG: expansion of processes and cell body, transformation into ameoboid form (like macrophages)
48
Q

motility of MG is governed by

A

the motility is governed partially by purinoreceptors & inhibition of astroglial gap junctions.

49
Q

activation of MG (process description)

A
  1. damage to the brain is detected by MG–> MG retract their processes–> 2. processes become fewer and thicker, soma size increases, expression of enzymes and receptors changes–> begin to generate immune response (activated MG)–> 3. MG become motile, ameoboid movements gather around damaged site–>4. (if damage persist) MG become phagocytic–> 5. after damage is fixed MG go back to resting form.
50
Q

types of activation signals for MG

A

off signals

on signals

51
Q

off signals

A

withdrawal of certain molecules (e.g. NT-GABA, Glu, Dopamine..)–> depression of NT release activate MG. when levels of NT release go up again, MG migrate away from damaged site)

52
Q

on signals

A

abnormal concentrations of molecules associated w. cell damage/invasion. specifically, damaged neurons can release high amounts of ATP, cytokines, neuropeptides, GFs–> trigger MG–>activation

53
Q

function of MG in synaptic pruning

A

MG play a role in the development of the brain, especially in the process of synaptic pruning (no. of synapses is reduces by MG’s phagocytic reaction that eliminate the excess synapses).

54
Q

function of MG during healthy states

A
  • neurogenesis
  • synapse monitoring
  • synaptic pruning
  • neuronal connectivity function
  • BBB permeability
  • myelination/remyelination?
55
Q

singling in astrocytes

A

signalling each other using ATP. The gap junctions between astrocytes allow the IP3 to diffuse from one astrocyte to another–> IP3 activates ca2+ channels on cellular organelles–> ca2+ released–> glial activation
The net effect is a calcium wave that propagates from cell to cell. (important for intercellular communication)

Medneuro- neurophysiology (M1-2) (6 decks)

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