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Dev Neuro > 4 > Flashcards

4 Flashcards

1
Q

What happens when there are more target areas and why.

A

Target areas make trophic factors that influence neuronal survival.

More targets means more neurons survival.

Adding an extra limb bud into an embryo causes more sensory and motor neurons to form.

Removing a target will increase the amount of cell death.
So targets don’t cause more growth. They limit cell death.

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2
Q

1948 sarcomas

A

Realised that fast growing muscle like cells might secrete survival factors.

Sarcomas are muscle tumours and they were implanted into an embryo next to its spinal cord. This caused an increase in the amount of neurons there.
The tumour cells were implanted generally. And they caused a general increase of neurons too.

This demonstrates the presence of NGF which is diffusible.

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3
Q

Where else can NGF be purified from

A

Snake venom

Mouse submaxilliary gland.

Sarcoma.

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4
Q

Using antibodies to block NGF function.

A

Caused a reduction in the size of the DRG in chick embryos.

NGF was not able to limit cell death.

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5
Q

NGF structure

A

Protein complex called 7S NGF

it has three types of subunit. Two alphas. Two gammas and one beta.

The active component is the beta subunit which is a dimer.

The other subunits are there for storage.

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6
Q

Campenot chamber

A

Axons can grow under small gaps at the bottom of the wall and pass into the other compartments.

If NGF is present in the chambers the cells will survive.
If NGF is only present in one chamber the cells will not grow out into non NGF chambers. And any axons already in there will retract back into the middle.

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7
Q

NGF

A

Affects cell survival and can guide growth cones.

Both tropic and trophic.
Chemoattractant.

Bind to its receptor and become internalised and transported to the soma by retrograde transport.

DRG soma take up NGF and it’s receptor when NGF is only given to its axons.

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8
Q

NGF receptors

A

The receptors have a high affinity component and a low affinity component. NGF can bind to either and give an effect.

Trka is the high. P75 NTR is the low.

Trka dimerises when NGF is attached to it. Ligand induced dimerisation. Then autophosphorylation leading to transcription.

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9
Q

Trka effect

P75 effect

A

Differentiation. Growth. Movement.

Promotes cell death or cell survival.

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10
Q

Why were more factors in the neurotrophin family hard to find.

A

They are all present in very low levels.

This is because they help cell survival so too much would cause cancer.

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11
Q

NGF

BDNF

NT3

NT4 5

What are they all first made as

A

Binds to trka and p75

Brain derived neurotrophic factor. Has a high homology with NGF. binds to trkb and p75.

Is a dimer. Binds to mostly trkc and sometimes trka and trkb.

Dimers.

They are all first made as pro proteins where an extra part has to be cleaved off before it is activated.

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12
Q

Where are NT6 and 7 found

A

Fish

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13
Q

P75

A

All of the neurotrophins can bind to p75.

It is promiscuous.

The NGF precursor called pro NGF can also bind to p75.

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14
Q

Which neurotrophin receptors are in control of which neuron types survival.

A

Trka- DRG, trigeminal

Trkc- DRG, trigeminal, cochlea, vestibular

Trkb- DRG, trigeminal, cochlea, vestibular and nodose

P75- 50% of the DRG

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15
Q

Receptors and their dependancies

A

Placode sensory ganglia - prefer BDNF or NT3

Crest derived DRGs can respond to NGF, BDNF, or NT3.

Sympathetic respond to NGF and NT3.

Merkels capsules have NGF NT3 and p75 at once.

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16
Q

How dependancy to neurotrophins changes over time.

A

Newly born neurons COULD have no dependency. They haven’t sent out axons yet so can’t respond to targets.

The neurons themselves make NT3 in early development to help them arrive at their targets. And it promotes differentiation

Arrival at the target causes expression of a new neurotrophin by the target.
Trigeminal neurons need BDNF and NT3 early, then NGF and then MSP.

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17
Q

Survival factors that aren’t neurotrophins

A

Drosophila and c elegans don’t have neurotrophins

Glia derived neurotrophic factors- GDNF supports midbrain dopaminergic neurons.

Cytokines- cilliary neurotrophic factor CNTF. Hepatocyte GF, macrophage stimulating protein MSP.

Testosterone gives more neurons in the genitals.

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18
Q

What else do target derived factors do other than help survival.

A

Form the monosynaptic stretch reflex.

The determine whether something is going to be mono or poly synaptic, gene expression.
The targets secrete GDNF which turns in the TF pea3 and allows poly synaptic connections.

Triceps and pecs have mono synaptic connections. Cutaneous maximus and lats have poly synaptic connections and interneurons.

The CM and lats release GDNF and turn on pea3.

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19
Q

Pea3 knock out

A

Neurons are mono synaptic.

No interneurons.

Aberrant connections

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20
Q

Target feedback with NT3

A

NT3 from muscles induces the expression of the TF er81 by Ia axons.

Knock out of er81 leads to no innervation if the ventral horn.

Feedback from the target determines the final pattern of both dendritic and axons connections.

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21
Q

What else can make neurotrophins other than the target.

A

Neurons

They can make them to support the synapses of other neurons next to them.

Anterograde transport. The target makes them for the neuron and the neuron makes them for the target.

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22
Q

Coordinated electrical activity.

A

Is a major determinant of survival.

The pre and post synapse have to be coordinated. If only one fires correctly it will cause reduced survival.

Inject curare gives more neuron survival.
This is because it stops activity and so will stop initiation of cell death mechanisms and allow more motor neuron survival.

It will block the asynchronous activity that would weaken the synapses. It does this by stopping activity all together.

Synchronous activity leads to strengthening of synapses and survival.

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23
Q

Synaptic competition

A

At first there are multiple neurons innervating one muscle.

This is then reduced by competition to a single neuron innervating a single muscle.

The neuron with the most synchronous activity will be strongest and survive. And the others will become weaker and die.

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24
Q

How to keep poly innervation

A

Block all activity

So the asynchronous activity can’t weaken any neurons and none will die.

So no neurons will lose the competition.

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25
Q

What converts electrical activity into survival.

How does this relate to target tissue mass.

A

The more active a synapse is the more neurotrophin it takes up by membrane recycling and this means it is more likely to survive.

The Greater the target mass the more neurotrophin that is available.

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26
Q

How to cause non synchronous firing

A

Do it experimentally and this will increase the rate if synaptic loss.

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27
Q

Do all neurons make synapses ?

Do all synapses persist

Are all synapses made in the same way.

A

No it is competitive

No

No. Some new and some regenerate.

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28
Q

To form a functional synapse-

5

A
  • correct receptors being expressed
  • synapses at correct location
  • receptors match the target tissue
  • the correct number of synapses is made
  • the correct part of the membrane becomes the synapse.
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29
Q

Innervation dependancy

A

Muscle spindles are dependant and they need sensory innervation to differentiate.

Merkel cell are independent and don’t need sensory input to differentiate.

30
Q

Morphological features of synaptic stabilisation.

A

Small vesicles at the pre synaptic membrane.

The synaptic cleft is narrow and fills with ECM

The post synaptic membrane appears thickened.

Can see on microscope.

31
Q

What changes when a growth cone turns into a pre synapse

A

The filapodia retract

Tight junction formation

Membrane and EC glycoproteins added

Presynaptic vesicles

Dense ECM and receptors accumulate in the cleft.

32
Q

Cat visual cortex

A

Synapse density increases at post natal day ten when they open their eyes.

33
Q

In vivo synapses

In vitro synapses

A

Take a while

Can form on contact.

34
Q

Muscle cell membrane onto a pipette

A

Muscle cell membranes have ach receptors.
The membrane on the end of the pipette is put near a growth cone.

Measure the amount of activity.
The closer the growth cone gets the higher the activity and more ach is released.

35
Q

What dictates synaptic sites

A

The approaching growth cone communicates with the target.

The astrocytes may cover up the cell body so there are fewer places to receive the target axon.

Post synaptic cells may have pre prepared sites.

Variety of cell adhesion molecules.

36
Q

Neuromuscular junction development

A

Poly innervation is refined to mono innervation.

Receptor clustering in the cleft

Increased transcription in cells receiving inervation.

Muscle cells are multi nucleate so the nuclei closer to the synapse will have increased transcription.

37
Q

Cause of receptor clustering

Examples.

A

The increased transcription increases the amount of receptor produced.

All types of receptor can cluster.

Glycine receptors use gephrin which binds to glycine receptors and clusters them together.

This is a principle feature of synaptogenesis.

38
Q

ARIA

A

Ach receptor inducing activity protein.

Released by motor neurons.

It increases the ach receptor mRNA and causes more transcription and production of the receptors.

Especially the E subunit. The E subunit replaces the gamma subunit in the mature form of the receptor.

It is a neuregulin and is found in the developing brain. They increase receptors.

39
Q

What evokes clustering.

A

Denervated and destroyed muscle.

Neuromuscular junctions form where basal laminate persist

40
Q

Agrin 4

A

A protein purified from T Californica because they contain many synapses.

Has multiple binding sites for ECM matrix proteins and adhesion.

Can be made by motor neurons and muscles.

All of the binding sites allows lots of molecules to stick together and promotes clustering.

41
Q

Agrin knock out

A

Causes death and malformed muscular junctions.

42
Q

Experiment to find which agrin is most crucial. Muscle or neuron agrin.

A

Chick motor neuron synapsed to a rat muscle.
Chick neuron releases agrin and rat muscle releases different agrin.

Antibody that blocks the chick neuron agrin is added.
Clusters can no longer be formed. Even though the rat muscle agrin is still functioning.

Antibody against the muscular agrin.
Clustering can still occur with only neuron agrin alone.

This means that neuron agrin is crucial for clustering.

43
Q

Mechanism of agrin action.

A

Agrin binds to muscle specific kinase MUSK

MUSK is bound to rapsyn which is bound to the ach receptor.

MUSK knock outs are not sensitive to agrin.

Without MUSK rapsyn will not pull the receptors and there will be no clustering.

44
Q

Rapsyn.

A

Ach receptors alone cannot form clustering.

Need rapsyn.

Rapsyn alone can form clusters.

Rapsyn KO means no clusters.

45
Q

Memories

A

The survival of the fittest connection theory is thought to apply to memories too.

46
Q

Hebbian synapse

A

Coordinated activity of the pre and post synaptic sides will strengthen the connection.

47
Q

Climbing fibre loss

A

In the cerebellum there are purkinje cells that when mature should only be connected to one climbing fibre.

During development up to four climbing fibres can attach to a purkinje cell.

One climbing fibre is favoured and it will shift its connections from the soma to the dendrites. The fibres that stay in the soma are killed off.

48
Q

Transmitter choice

Two factors

A

Environment (can cause neurons to change which transmitter that make)
Implanting adrenergic neurons into a cholinergic neuron site will cause them to become cholinergic.

Targets can change which transmitter the neuron works with.
A tissue transplanted into an area with neurons that have the wrong ntms for it can cause the surrounding neurons to work with its transmitter of choice.

49
Q

Turning on synapses

A

Silent synapses- fully formed but has no electrical activity.

Applying very high electrical stimulation for a short time can result in long term potentiation and the synapse will turn on.
The synapse activity will be enhanced and stronger.

AMPification- Activate silent synapses. NMDA
When the initial synapse forms the receptors are blocked and won’t work.
The high frequency stimulation will depolarise the membrane and drag mg ions our id the receipts and allow ca release.
This upregulates AMPA receptors instead of NMDA.

50
Q

How many traumatic injuries happen in the PNS

A

300,000 per annum

51
Q

Which animals have a higher regenerative ability

What triggers xenopus tadpole tail regeneration

Severing newts limb

A

Lower vertebrates. Reptiles and amphibians and fish.

Triggered by BMPs.
Until a critical Period in development is reached and they can no longer regrow their tails until after.

Grows back proximal or distal chop.

52
Q

Cutting off of limb leaves

A

Blastema stump

Bud of cells. Mainly stem cells.

The nerves close to the blastema will cause Schwann cells to migrate to the blastema and interact to allow regrowth

In most cases a nerve is required to drive regeneration.

53
Q

Layers in a nerve

A

Axon is surrounded by Schwann cell and endoneurium

Many axons make a fascicle which is surrounded by perineurium.

Many fascicles form a nerve which is surrounded by epineurium.

54
Q

Neuropraxia

Axonotmesis

Neurotmesis

A

Damage produced by compression or stretching. It damages the myelin and Schwann cells so the insulation is reduced but that is all.

Axon is divided. Connective tissue is ok. No impulses can travel.

Nerve is completely divided. Axon and connective tissue are separated and it very rarely heals alone.

55
Q

PNS damage and where it is on the axon.

A

Close to the soma means likely death.

Far from soma/distal end allows reorganisation and rexpression of immature features like Tubulins.

The distal end of the axon starts to fall apart which is called wallerian degeneration.
This is required for repair
Macrophages come in and degrade the damaged end
The proximal axon and soma are able to regenerate.

The dendrites retract

56
Q

Damage to neuron innervating a muscle

Effects and how to avoid

A

The distal end of the nerve connect to the muscle so when it is degenerated the muscle will no longer be innervated and this will cause muscle atrophy.

Immature molecules will start to be expressed.
Embryonic ach receptors are found.
Increase in MUSK.

The atrophy can be avoided if you can artificially provide electrical stimulation to the muscle.

57
Q

What does PNS nerve regeneration involve.

A

Small damage/neuropraxia

  • mitosis of Schwann cells
  • provide many growth factors
  • arrange themselves into rows forming the bands of bungner
  • they will provide axons for the new axon to grow onto. And guide their growth by forming new connective tissue
  • sprouting- neighbouring fibres grow and reinervate the damaged axon
58
Q

Crush injures vs cut

Surgery

A

Crush injuries normally preserve the basal lamina and ECM.

Cut injuries will disrupt the basal lamina and ECM.

Crush injuries are easier to heal because the Schwann cells are able to produce the bands of bungner

Surgery- join axons with a large gap. Design a scaffold tube to make a bridge to connect them although they may not grow back correctly.

59
Q

Spinal cord injuries

A

Try sprouting

Nearly always fails

60
Q

PNS vs CNS regeneration

A

PNS are better
CNS can but poorly.

The CNS has oligos instead of Schwann.
Removing oligos improves regeneration.

Autoimmunity to myelin improves regeneration.

Myelin proteins are thought to prevent neuron growth.

61
Q

NOGO

A

NOGO-a is 200kd

In oligos and developing neurons

NOGO b and c too

Fish and salamanders lack NOGO a

Knockout of NOGO a prevented it inhibiting neuron growth and this partially improves regeneration.

62
Q

Motor recovery in spinal cord

A

Partial lesions may be fairly recoverable.

Wallerian degradation in the CNS is a lot slower.

63
Q

NOGO a suppression

A

Improves motor recovery in rats.

There is no correlation between NOGO and the amount of regeneration.

Some transplanted hippocampal neurons grow their axons into myelin even though it contains NOGO.

And regeneration does not improve when myelin is removed by macrophages.

So myelin isn’t the only thing preventing regeneration.

Regeneration is poor in grey matter too which has no myelin.

64
Q

The wrong glia

A

Thought to cause poor regeneration in CNS.

A glial scar will form during healing which contains astrocytes.
Astrocytes are thought to inhibit axons growth.

They can form cavities that axons can’t grow through because they can’t find their way and it contains the wrong ECM.

Secrete inhibitory things.

65
Q

Spinal cord bridges

A

Putting structures in the spinal cord that will bypass the scar.

Filled with growth factors and ECM.

66
Q

Four ways to repair

A

Transplant foetal cells-
For Parkinson’s it had conflicting results and side effects.
Not great results for Huntington’s.

Human embryonic stem cells-
Great potential for Parkinson’s.

Umbilical cells-
Not similar enough to neurons.

Autologous NS stem cells-
Found in adult body.

67
Q

Male songbirds

A

Sub ventricular zone in the brain

Learn to sing by the division of cells and making new neurons.

This is found in humans but is less advanced.

68
Q

Olfactory ensheathing cells

A

In rodents the olfactory bulb is producing many new neurons.
In humans this is less developed.

Human olfactory nerves are surrounded by olfactory ensheathing cells similar to Schwann cells. They can make new neurons.

You can extract these cells and clone them and put them back into patients who have few olfactory neurons
Or into the spinal cord to repair it.

69
Q

Breeding a mouse that has tissue specific knock out

A

One mouse has the gene to be knocked out and loxp sites are introduced on either side of it.

Another mouse has cre recombinase expression but only in the heart because of a specific promoter

They are crossed. The offspring has the gene only knocked out in the heart because cre recombinase an only cut the gene out in the heart.

70
Q

What do commisural axons eventually give rise to.

A

Sensory relay axons

Noci thermos and mechano info

Into the somatosensory cortex

Dev Neuro (7 decks)

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