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Neuro BSc > Module 1 - cells > Flashcards

Module 1 - cells Flashcards

1
Q

Define a PNS/CNS neuron

A

Peripheral neurons have their cell bodies
outside the brain or spinal cord, and
Central neurons have their cell bodies within
the brain and spinal cord.

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2
Q

Define neurulation and where the CNS and PNS neurons come from

A
  • formation of neural tube and crest
  • CNS neurons arise from the
    neuroectoderm following closure of
    the neural tube.
  • PNS neurons arise from the neural
    crest that overlies the neural tube
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3
Q

How do different neuronal populations arise?

A
  • 2 apposing morphogen gradients
  • SHH produced by floor plate,
    ventral to dorsal gradient
  • BMP4 produced by roof plate,
    dorsal to ventral gradient
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4
Q

Where do pyramidal neurons originate from?

A

Dorsal ventricular zone - radial migration

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5
Q

Where do interneurons originate from?

A

Medial ganglionic eminence - tangential migration

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6
Q

Describe somal translocation

A

Translocating cells possess a long pia-directed process that has a stable attachment at the pial surface or
marginal zone. Continuous speed 60mm/h

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7
Q

Describe locomotion

A

Locomoting cells have a short, constant leading
process and migrate along radial glial guides which they contact. Short bursts followed by stationary phases (30mm/h). Switch to somal translocation once pia attachment.

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8
Q

Give examples of somato-dendritic specific components:

A

Microtubule stabilising protein MAP2B
All the neurotransmitter receptors, postsynaptic
density (PSD) scaffolding and signalling proteins
required at the post-synapse.

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9
Q

Give examples of axon specific components:

A

•Neurofilaments are only present in axon, where
they are important for strength.
•Microtubules are aligned and stabilised
•Microtubule stabilising protein tau
•Cell adhesion molecules L1 (NgCAM), TAG-1
•All the neurotransmitters, growth factor receptors,
SNARE complexes, etc required at the presynapse.

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10
Q

What are axon collaterals?

A

Branches from axon after leaving cell body and extensively at target. Same diameter along axon (apart from axon hillock)

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11
Q

Which channels are found in which areas around the Nodes of Ranvier?

A

K+ channels in Juxtaparanode
Na+ channels in nodal region
Caspr-1 in paranodal region.

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12
Q

Name two types of synapses:

A

Boutons and varicosities

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13
Q

Axo-dendritic synapses are usually…
Axo-somatic synapses are usually…
Axo-axonic synapses are usually…

A

excitatory.
inhibitory.
excitatory.

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14
Q

Where are competing inputs integrated?

A

Postsynaptic neuron.

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15
Q

Where do astrocytes develop from?

A
  • initially astrocytes derive from neuroepithelium via radial glia
  • later astrocytes derive from migratory precursors from the SVZ
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16
Q

Astrocytes develop from which domain of the ventral neural tube?

A

p2, not SHH dependent, produce Fgfr3

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17
Q

How do astrocytes communicate?

A

GAP junctions (connexin 43)

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18
Q

How does inflammation in the subarachnoid space affect astrocytes?

A

Disrupt glia limitans.

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19
Q

What are Bergmann glia?

A

A type of radial glia - the granule cell neurons of the external granule cell layer migrate along the Bergmann glia to reach the internal granule cell layer.

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20
Q

Discuss the role of radial glia as stem cells?

A

Radial glia can give rise to neurons, astrocytes and ependymal cells – seem multipotential. Even mature astrocytes seem to have the capacity to form neurons.

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21
Q

What are two terms for dysmyelination syndromes? Give an example.

A

Leukodystrophies and leukoencephalopathies.

Folate receptor defect, Globoid leukodystrophy, vanishing white matter disease, etc.

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22
Q

Where do oligodendrocytes originate from?

A

Subventricular zone cells (brain and spinal cord)
- SHH produced by floor plate (notochord before floor plate) ventral to dorsal gradient
- BMP4 produced by roof plate (ectoderm before roof plate), dorsal to ventral gradient
Nx2.1 expressing areas first (medial ganglionic eminence, to whole cortex) (eventually completed ablated after other waves), then Gsh2 (lateral ganglionic eminence) and then Emx1 (cortex) (Kessaris 2006)
The last two waves are more dorsal and are independent of Shh and Nkx6 (Cai 2005)

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23
Q

Describe how the genes/transcription factors interact with the domains for oligodendrocytes.

A

Olig2 + Nkx6.1 (and lack of Nkx2.2 and Nkx2.9) -> pMN domain -> motor neurons and OPCs
OPCs specifically because no Ngn1 and 2 and Nkx2.2 starts to overlap with olig2
If Nkx6 null, OPCs from dorsal areas (Pax7 and Msx-3 expressing regions) only, usually suppressed by ventral OPCs

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24
Q

What transcription factor do all malignant gliomas express?

A

olig2

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25
Q

What happens to olig1 null mice?

A

Die at 3 weeks.

Oligodendrocytes mature later and can’t myelinate axons.

26
Q

What happens to olig2 null mice?

A

No oligodendrocytes in spinal cord (some in brain stem, unless no olig1 either)
No motor neurons
Phosphorylation olig2 -> motor neuron shift, dephosphorylation -> oligodendrocyte shift (Lu 2002)

27
Q

What is the effect of platelet derived growth factor on OPCs?

A

Promotes proliferation, survival and migration in a dose-dependent manner (Calver 1998)

28
Q

What is the effect of fibroblast growth factor 2

A

Promotes proliferation and migration and inhibits differentiation.

29
Q

What is the effect of neuregulin beta1

A

Promotes proliferation, target dependent survival and myelin formation.

30
Q

What intrinsic or extrinsic factor has the biggest impact on myelination?

A

Axon contact.

31
Q

What transcription factors affect myelination?

A

Ying Yang 1 inhibits the inhibitors (Sox5,6, etc.) (He 2007)
Activators: Sox10, Olig1,2, etc.
The master transcriptional regulator = Myelin Gene Regulatory Factor, CNS, nuclear protein expressed in post-mitotic oligodendrocytes, null mice die at 3 weeks (Emery 2009)

32
Q

Describe how the oligodendrocyte makes contact with the axon:

A

Oligodendrocyte and axons both express NCAM (or N-cadherin, L1, neurofascin-186) (a type III fibronectin repeat with an Ig domain) associated with an FGF receptor.

33
Q

Describe how the oligodendrocyte maintains contact with axons and ensheath them:

A

Electrical activity in the axon causes ATP release which stimulates astrocytes to secrete leukaemia inhibitory factor (LIF)
There is also direct stimulation of oligodendrocytes through the NCAM contact.
Inhibitory molecules are downregulated (Notch, PSA-NCAM, Lingo-1).
More axo-glial signals which causes ensheathment. (Ishibashi 2006)

34
Q

How does the oligodendrocyte ensheath the axon?

A

Leading process underneath and round, multiple layers, spread laterally too and create septate junctions. This creates myelin compaction.
After myelination, all unnecessary processes retract (Trapp 1997)
Dark lines = compacted intra-cellular faces of the membrane (lots of proteins, especially PLP)
Lighter lines = compacted extracellular faces of the membrane (Sherman 2005)

35
Q

Discuss the role of oligodendrocytes in adult brains:

A

Still proliferate new oligodendrocytes, create new myelin, (because new skills?) and remodel existing myelin in optic nerve (Young 2013)

36
Q

What is the relationship between Schwann cells and axon segments?

A

1:1

37
Q

Where do Schwann cells originate from?

A

Ectoderm -> neural crest (because Wnt, BMP and FGF)

38
Q

What transcription factors promote neural crest -> Schwann cell precursor? Which promotes Schwann cell precursor -> immature Schwann cell?

A

FoxD3 and Sox10.
Schwann cell precursors can also turn into melanocytes, endoneurial fibroblasts and parasympathetic neurons and die without axonal contact or neuron conditioned medium. (Jessen 2015)

39
Q

What does neuregulin 1 type III do?

A
  • found on axons
  • Promote Schwann cell precursor -> immature Schwann cell
  • potent mitogen
  • Level decides if myelination or not and how much myelination (Jessen 2015)
40
Q

What pathways can an immature Schwann cell take?

A 
Radial sorting -> promyelin cell -> myelin Schwann cell
OR Nonmyelin (remak) Schwann cell
once a myelin or nonmyelin Schwann cell, there is an intermediate of a repair (bungner) Schwann cell which can go either way. (Jessen 2015)
41
Q

How does a Schwann cell and axon make contact?

A

Neuregulinbeta expressed from axon acts of ErbB2/3 receptors on Schwann cell BUT Schwann cell gives axon a survival factor back - not sure what yet.

42
Q

What mitogens are expressed by axons for Schwann cells?

A

Neuregulin 1 type III and TGFbeta.

43
Q

Which cells take over the smaller axons once a large axon and myelin Schwann cell have been paired off?

A

Immature Schwann cell differentiates into a nonmyelin Schwann cell to take the little axons.

44
Q

How are myelin proteins in a Schwann cell activated?

A

Something activates the Gpr126 receptor on a Schwann cell which creates an increase in intracellular cAMP which stimulates PKA -> Sox10 ->Oct6 -> Krox 20 (although Oct6 affected by ErbB2/3) Oct6 and Krox20 -> myelin proteins (eg. Pzero, MBP, etc.) but myelination can happen without Oct6 (not without Krox20) (Jagalur 2011)

45
Q

What is the function of neurons?

A
  • information processing unit.

- responsible for the generation and conduction of electrical signals.

46
Q

What is the morphology of neurons?

A

Diversity of morphology determined by location and function
Polarised cell, different compartments of:
- Dendrites (location of branches determines the origin of the incoming signals, spread from cell body and branch frequently, covered in spines)
- Dendritic spines
- Axons - Axon hillock (initial segment)
- Myelin sheath
- Nodes of Ranvier
- Paranode and juxtaparanode
- Synapses
- Pre-synaptic terminals
- Post-synaptic specialisations

47
Q

What is the intracellular architecture of neurons?

A
  • large nucleus
  • prominent nucleolus
  • abundant rough ER and free ribosomes (secretory pathway protein trafficking)
  • well developed Golgi
  • abundant mitochondria
  • highly organised cytoskeleton
  • HIGHLY ORGANISED METABOLICALLY ACTIVE CELL
48
Q

What is the function of astrocytes?

A
  • function as a syncytium that allows spreading of reaction and signalling.
  • myriad of fine processes sample the microenvironment and interact with other cell types.
  • Astrocytic endfeet enwrap endothelial cells, providing the gateway for nutrients etc into the CNS, and removal of metabolites from the CNS.
  • Express : transport proteins for nutrients (eg glucose) and metabolites, neurotransmitter transporters (glutamate, GABA etc) and receptors, neuronal trophic factors (GDNF, FGF, IGF)
  • well placed to modulate neuronal function via transmitter removal and also release, closely associated processes with synapses. (eg. GABA  glutamic acid + amine  glutamine for neuron)
  • Remove potassium ions from extracellular space – essential for neuronal function, since extracellular potassium concentration must be kept low. After intense neuronal activity, local concentrations of potassium can become very high. Potassium is redistributed from these regions to other regions, by transport through the astrocytic network via gap junctions. Thus they play a role in “spatial buffering” of potassium. Astrocytes therefore act as a potassium reservoir, maintaining a good supply of potassium, but keeping it away from the extracellular space until required.
  • Gap junctional connections allow exchange of ions and small molecules < 1kDa
  • Glycogen stores – give lactate to neurons for energy
  • AQP4 – pressure control?
  • control cerebrovasculature via arachidonic acid & prostaglandins (constrict and dilate)
  • neural stem cell?
49
Q

What is the intracellular architecture of astrocytes?

A
  • Cytoskeleton - IF GFAP,microtubules, actin.
  • glycogen granules
  • Rough ER, Golgi apparatus
  • Large nucleus.
  • Light cytoplasm
50
Q

What is the distribution of astrocytes?

A
  • ordered arrangement of astrocytes with minimal overlap
  • each cell forms a specific territory that interfaces with microvasculature
  • might include thousands of synapses in grey matter and multiple axons in white matter
51
Q

Define a true microglia:

A

Mononuclear phagocytes of the CNS. Only true if in the parenchyma. (Ie. perivascular macrophages in perivascular space of parenchyma and blood doesn’t count and neither does choroid plexus macrophages nor meningeal macrophages in CSF over surface of brain.)

52
Q

What is the function of microglia?

A

Immune surveillance of CNS.
Provide trophic support for neurons.
Remove cellular debris from PCD and axonal projections.
Drive PCD in foetal brain remodelling and the pruning &
elimination of synapses via C3-CR3 signalling and maturation of synapses via CX3CL1/CX3CR1 .
Passively monitor synapses by surrounding neuronal soma (can decrease firing)

53
Q

What is the distribution of microglia?

A

10%, ubiquitous

54
Q

What is the morphology of microglia?

A

High ramified in health
Amoeboid in disease.
Hyper-ramified in noxious stimuli eg. chronic stress

55
Q

Where do microglia originate from?

A

From yolk sac myeloid cells (common myeloid progenitor) at embryonic stages. (Ransohoff 2010)
Know this because PU.1 for myeloid cells, null PU.1 - no microglia.
If irradiate, then microglia from host’s bone marrow (monocytes) (Vallieres, 2003) but tends to be more M1. (Yamasaki 2014) Axotomy and MND showed this population too (Ajami 2007)
Appear at the same time as vasculariation in foetus.

56
Q

What marker is high in macrophages and low in microglia?

A

CD45 (and CD11b+)

57
Q

How do microglia carry out immune surveillance?

A

Static (not migratory) but motile processes retract and extend to sample local environment. (Nimmerjahn 2005) They also have contacts with neurons, astrocytes, blood vessels and dendrites and synapses.

58
Q

Describe the immunological activities of microglia:

A

Recognise micro-organism through carbohydrate and
lipid motifs with PRRs, CR3 or Fc receptors
Phagocytose microbes (cell lysosomes of microbiocidal oxygen metabolites and enzymes)
Cytokines, APC, pro-inflam. and anti-inflam. markers, PAMPs
Activated microglia upregulate MHC II for T cells

59
Q

How do microglia promote neuronal repair?

A

Axotomy: Fractalkine or massive ATP release from cell body
Microglial response with proliferation, release TGFbeta, displace axosomatic terminals (deafferentation)
Once target reinnervates, microglia die by apoptosis (Moran 2004)

60
Q

How do neurons keep microglia quiescent?

A

Fractalkine (activation), electrical activity (antigen presentation), CD200 (neurons) -CD200R (microglia) (activation)

61
Q

What are some differences between M1 and M2 microglial cells?

A

M1 polarised microglia produce:
TNF, IL1β, IL6, IL12, CCL8, CXCL9/10, CCR7, CD80
M1 polarised microglia express:
MHC class II, CD68, iNOS
M2 polarised microglia produce:
IL10, IL4, CCL1/20, CXCL1/13, TGFβ, BDNF, IGF, CD209, CD163
M2 polarised microglia express:
Arginase 1, Ym1 (heparin binding lectin), mannose receptor

Neuro BSc (16 decks)

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