Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neurobiology of Repair & Degeneration > Anderson CNS HIstory > Flashcards

Anderson CNS HIstory Flashcards

(58 cards)

Start Studying
1
Q

When an axon is injured, the distal portion dies, how is death regulated and what does depend on?

A

Neuron can either:
1.DIE
2.DO NOTHING
3.REGENERATE

Depends on type of neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where can axons regenerate

A

In adult mammalian peripheral nerves
axonal sprouts regenerate and regrow along pre-existing fibre hoepfuly join to target organ and continue function.

It is hard to stop them regenerating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How many axons are there post injury?

A

More axons post injury (conditioned lesion effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Axonal regeneration in species ranking

A

Axonal regeneration in fish>amphibians>reptiles>mammals
but even in mammals some functional recovery may be achieved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What structure guides regenerating axons in peripheral nerves?

A

Band of Büngner (formed by Schwann cells).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Wallerian degeneration?

A

Degeneration of axons and myelin distal to injury; cleaned up by Schwann cells and macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which cells form the band of Büngner?

A

Schwann cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name 4 growth-associated genes upregulated after peripheral nerve injury

A

GAP-43
CAP-23
SCG10
SPRR1A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What transcription factor is essential for peripheral nerve regeneration?

A

C-Jun

KO study showed this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the ‘conditioning lesion effect’?

A

A prior injury enhances future axonal regeneration by priming gene expression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens to neonatal neurons after PNI?

A

High likelihood of cell death and poor regeneration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is CNS axon regeneration poor? Give 3 reasons.

A

Weak cell body response, lack bands of bunger and inhibitory environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What molecules in CNS inhibit axon growth?

A

Nogo-A, MAG, OMgp, CSPGs (e.g., NG2, tenascins).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What CNS neurons regenerate well into peripheral grafts?

A

Thalamic reticular neurons (TRN), rubrospinal, retinal ganglion cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the typical regeneration rate of human peripheral axons?

A

About 1 mm per day.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the role of macrophages in nerve injury?

A

Remove debris and may promote regeneration via signals like oncomodulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What gene deletion enhances optic nerve regeneration?

A

PTEN and SOCS3 double deletion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the role of integrins in regenerating neurons?

A

Aid in adhesion and axon guidance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What effect does chondroitinase ABC have?

A

Digests CSPGs, improving axon regeneration in CNS injuries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What characterizes a poor CNS regenerator neuron?

A

Weak or transient upregulation of growth-associated genes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the effect of anti-Nogo-A treatment?

A

Enhances functional recovery after CNS injury (especially partial lesions).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a major reason CNS lesion sites enlarge instead of healing - slow wound healing?

A

lack of intrinsic regenerative ability in the CNS, the formation of glial scars that act as barriers to regeneration, and the absence of Schwann cells, which support axonal regeneration in the peripheral nervous system.

Additionally, the inflammatory response and the presence of inhibitory molecules in the glial scar can further impede recovery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What distinguishes Schwann cells from CNS glia in injury response?

A

Schwann cells dedifferentiate, proliferate, and support regrowth; CNS glia often inhibit regrowth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the regenerative capacity of peripheral nerves dependent on?

Study These Flashcards
A

distance from cell body and age of the animal

25
Which type of peripheral nerve injury in rodent causes neruonal death the most
neonate both distal and proximal causes cell death and no conductive nerve regeneration
26
What is the regenrative capcity of neonate humans following injury
more regenerative capacity than rodents
27
Which genes are downregulated following PNI?
Neurofilament Neurotransmitter-related ATF2
28
Why is the cell body response so important for axonal regeneration?
Cell soma activates signalling pathways involved in regeration, Knockout studies show without it, regenration does not occur e.g. c-jun
29
What happens if axons were cut distally and proximally in Peripheral root and axon?
Regeneration in the dorsal root is vigrous but most axons would not enter spinal cord
30
Why is functional recovery NOT guaranteed following suturing a PNI
Regenerating axons get lost and do not go to target.
31
When do axons begin regeneration following PNI
With a few hours not all axons start regnerating immediately
32
Which cells migrate across gap from distal stump to heal the wound
endothelial cells, schwaan cells
33
What gaps size can axons regnerate acorss
10mm in rodents with or without conduits
34
How can you imporve regenration across gaps
Porous tubes to allow outside cells to come in to help e.g. macrophages
35
What process do axons distal to inury undergo?
Wallerian degeneration Axons and myelin are phagocytosed by macrophages and Schwann cells
36
Roles of shwaan cells in wallerian degeneration?
* Dedifferentiate * Proliferate (Abercrombie-UCL, 1940’s) * Help to remove debris * Develop regeneration-supporting phenotype? * Put out many long processes * Migrate into lesion site * Up-regulate some neurotrophins (NGF, BDNF, NT4, not NT3) and other trophic molecules (pleotrophin, IGF) * Release cytokines (LIF, CNTF) * Up-regulate tenascin-C and tenascin-Y
37
Where are Bands of Bunger not found?
CNS
38
Which cell adhesion molecules promote neurite growth in vitro + location
L1, NCAM - found between SCs and axons
39
Which molecules are repulsive to neurites in vitro + location
NG2, tenascin C - found in basal lamina ad endoneurial spaces outsdie basal lamina
40
What can penerate basal lamina and how do we know that
growth cones We know through partial denervation
41
What are the 3 limitating factors for CNS injury response
1. Inadequate cell body response to axotomy 2. Inhibitory factors in CNS 3. Inadequate neurotrophic support (and no bands of Büngner)
42
What is absent in the CNS after injury
Bands of bunger Wound healing
43
What happens following CNS instead of regeneration
increased cavitation and slow incomplete wound healing
44
What are the 4 inhibitory molecues in glial scar following CNS?
* Chondroitin sulphate proteoglycans CSPGs * NG2 * Tenascins * Collagens * Developmental axon guidance molecules (ephrins, semaphorins, slits) * Fibrinogen (enters the CNS following injury)
45
Do CNS neurons show an inadequate cell body response to axotomy?- experiment
Anterograde tracing after transplant of CNS tissue in PNS enviroment showed they can regenerate following injury- so due to milleu
46
What are the 4 poor regenrators in CNS?
Most forebrain neurons including: 1.Thalamic projection neurons 2. Cerebral cortical projection neurons 3. Striatal projection neurons 4. Cerebellar Purkinje cells
47
What are the 8 good regenrators following CNS
* TRN * Deep cerebellar nuclei * SNpc * Cholinergic CNS neurons * Rubrospinal neurons * Retinal ganglion cells * Raphe-spinal neurons * (Most spinal cord neurons)
48
Which cells types spontaneously regenerate after CNS injury without treatment, inclu caveat
Retinal ganglionic cells after crush optic nerves (but most RGCs die after axotomy) Raphespinal axons 5HT in spinal cord
49
What method had been tried to improve regenration in CNS injury
Improving cell body response or delivering growth associated genes to non-regenerating neruons * Ascending dorsal column axon regeneration into nerve grafts in the spinal cord is greatly enhanced in mice overexpressing GAP-43 AND CAP-23 in DRG neurons * Purkinje cell axon regeneration is enhanced by overexpressing GAP-43 AND L1 * Lentiviral vector delivery of retinoic acid receptor ß2 promotes recovery of function after corticospinal tract injury in the adult rat spinal cord * But overall the results have not been spectacular- not surprising when one considers that many hundreds of genes are regulated in successfully regenerating neurons
50
Which 3 inflammatory agents enhance axonal regeneration following CNS injury?
Oncomodulin Stromal cell-derived factor (SDF)-1 Chemokine CCL5
51
Is inflammation nessary to help axonal regeneration?
Not always- when they reduced it, axonal regenration still occurs. Mice lacking MCSF show impaired microglial activation and lymphocyte recruitment but no effect on axonal regeneration Hypoglossal nerve axons regenerate normally in rats in which the microglial cell reaction is blocked by cytosine arabinoside
52
What were different groups opinions about anti-NOGO?
* Strittmatter’s group: regeneration of corticospinal axons claimed * Schwab’s group: a little regeneration of CSTs claimed * Tessier-Lavigne’s group (and Zheng): no regeneration
53
What is the difficulty about targeting NOGO inhibtiory
NOGO has multiple receptors, may need to be targeting them all
54
What is the best evidence that mylein is not inhibitory to regeneration
The strongest proof that myelin doesn't block nerve regeneration in the CNS comes from experiments where adult DRG neurons are transplanted and grow axons through white matter just as quickly as they do in peripheral nerves."
55
Which recpetor does inhibtory molcule CSPGs bind to
(protein tyrosine phosphatase sigma) PTPσ
56
What happens when you KO PTPσ
PTPσ−/− neurons show reduced inhibition by CSPG. After spinal cord injury, PTPσ gene disruption enhanced the ability of axons to penetrate regions containing CSPG. Adult PTPσ–/– sensory neurons show reduced sensitivity to inhibition by a proteoglycan gradient but cannot regenerate axons through a spinal cord lesion in vivo
57
Whihc inhibitry meolcues has contrversial findings in vivo versus in vitro
In vitro studies show NG2 is inhibitory NG2 is never found on astrocytes in vivo And knocking out NG2 results in absolutely no increase in regeneration in the spinal cord
58
Problem of replicability
spared axons

Neurobiology of Repair & Degeneration (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions