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Neuro Science > Degeneration and Regeneration Recovery of Function > Flashcards

Degeneration and Regeneration Recovery of Function Flashcards

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1
Q

Degeneration in the PNS

A
  1. Axon is cut (in this case, complete separation)
  2. Proximal and distal ends of axon seal off the leaking axoplasm and swell [close off fast]
  3. Rapid degeneration of axon and myelin sheath away from the zone of injury [towards axon]
  4. Blood vessel damage- can cause more swelling, which can cause more compression and further the injury
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2
Q
  1. Macroglia & microglia cells …
A

-PNS Degen.
-absorb and destroy debris
-Macroglia
Schwann cells (PNS)
Oligodendrocytes (CNS)
Astrocytes (CNS)
-Microglia (CNS)

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3
Q
  1. Glial cells…
A

proliferate and form glial scar tissue [can deflect the newly growing axons-so want to prevent them from growing too much scar tissue]

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4
Q
  1. Orthograde degeneration (Wallerian)….
A

-Degeneration “distal” to zone of injury (away from cell body*)
-Begins immediately
–Glial cells push old axon away from post-synaptic target
Entire distal axon degenerates (axon and myelin phagocytized)

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5
Q
  1. Retrograde degeneration
A
  • Degeneration “proximal” to zone of injury (toward cell body*)
  • Up to 1st axon collateral or only 1-2 nodes of Ranvier
  • If site of lesion is close to the cell body -> the neuron may die
  • If distal to cell body, neuron may live if it properly reconnects to the target tissue
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6
Q

Transneural Degeneration

A

secondary neuronal death of neurons more “proximal” or “distal” to/from the damaged neuron along the neural pathway

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7
Q

Amount of transneural degeneration is dependent on the number of neurons prior to or AFTER the injured neuron

A

Ex: if damaged neuron was one that had multiple axon branching or synapsed on multiple 2nd order neurons > result is widespread orthograde transneural degeneration

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8
Q

Amount of transneural degeneration is dependent on the number of neurons PRIOR TO or after the injured neuron

A

Ex: If damaged neuron was a 2nd order neuron that had multiple 1st order neurons synapsing on it > widespread retrograde transneural degeneration

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9
Q

Transneural Degeneration: Potential mechanisms

A
  • Some type of trophic interaction between neurons to maintain the chain’s health
  • Maybe that working electrochemical circuit is necessary to maintain chain’s health
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10
Q

Recovery of Function

A
  • No single mechanism accounts for all of the recovery phenomenon following a lesion of a nerve.
  • Recovery results from the collective contribution of several mechanisms toward a common goal of reorganization.
  • This supports the idea of using as many of the intervention approaches as possible to tap into all of the recovery of function mechanisms.
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11
Q

Early Mechanisms of Recovery

A 
Resolution of:
spinal shock,
edema or blood clot,
diaschisis
unmasking of redundant pathways

are probably mechanisms for early recovery of function

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12
Q

Spinal Shock

A
  • transient suppression of all reflex and motor activity below the level of the lesion
  • is an immediate effect of spinal damage
  • initial stage
  • -body below the level of the lesion is paralyzed & anesthetized
  • -Autonomics are suppressed; loss of circulatory tone, urine retention, and anhidrosis (absence of sweating)
  • later stages
  • -some/any reflex activity returns in somatic and autonomic structures
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13
Q

Spinal Shock Duration

A

Duration:
-species dependent

  • Subsequently - reflexes become exaggerated; hypertonicity
  • Resolution of spinal shock > recovery
  • –Presence of spasticity means period of spinal is ending or has ended.
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14
Q

Early Transient Events that Depress Brain Function: Edema

A
  • Common response following brain injury
  • Edema can be local or remote from the site of injury
  • may compress neuron’s cell body or axon, causing focal ischemia, which disrupts neural function, including synthesis and transportation of neurotransmitter.
  • Eventually the synapse become inactive and silent.
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15
Q

Cytogenic edema

A

accumulation of intracellular fluid

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16
Q

Vasogenic edema

A

proteins and fluid leaking from damaged blood vessels

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17
Q

Diaschisis

A
  • “Diaschisis is a transient CNS disorder involving loss of function … because of loss of input from an anatomically connected injured area of the brain.”
  • “The sudden functional depression of brain regions distant from the primary site can be due to a reduction in blood flow and/or metabolism.”
  • “It has been proposed that early recovery of function following stroke is due to the resolution of diaschisis”
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18
Q

Diaschisis in the…

A

inhibition or the depression

of other neural networks.

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19
Q

Redundancy of ineffective synapses, silent synapses or latent pathways….

A
  • Parallel pathways that may perform the same or similar functions may be unmasked
  • Good example: Damage to the Lateral CST; parallel motor pathways include the anterior CST, Rubrospinal tract, RST, VSTs
  • Takes time for the unmasking to occur
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20
Q

Multiple mechanisms underlying “LATER” Recovery of Function

A
  1. Collateral sprouting
  2. Regeneration or regenerative synaptogenesis
  3. Pre-synaptic compensatory response
  4. Denervation Supersensitivity
21
Q
  1. Collateral sprouting (takes time)
A
  • When partial denervation to a target site occurs, the remaining neurons branch to occupy “old, damaged” sites and form synapses. Results in fiber-type grouping.
  • Axon of a remaining neuron forms a collateral sprout to reinnervate denervated target
  • End Result: leads to less control b/c 1 giant motor unit is controlling a mm instead of 2 separate neurons
  • Sprouting occurs in the PNS and CNS of higher vertebrates
22
Q
  1. Neural Regeneration
A
  • Recovery mechanism
  • Presynaptic axon is damaged
  • Injured axon sprouts to new targets
23
Q

what may collateral sprouting inhibit?

A

may inhibit restitution of the original innervation pattern

24
Q
  1. Pre-synaptic compensatory response
A
  • More release of neurotransmitter per pre-synaptic membrane to compensate for damage
  • Ex: PD- clinical symptoms only appear after approximately 80% of dopamine producing cells have degenerated (substantia nigra)
25
Q

Aberrant regenerative sprouting in PNS

A

-Axon sprouting can cause problems when inappropriate targets are innervated.
-After injury, motor axons innervate different muscle than they previously did, causing unwanted abnormal movements
[Ex: Bell’s Palsy]
-Usually lasts no more than a few months

26
Q
  1. Denervation Supersensitivity
A
  • Occurs when neurons lose input from another brain region, e.g. postsynaptic neurons in the striatum become super-sensitive to dopamine in pt with PD
  • “spread out” and make a larger target and are more sensitive to any neurotransmitter
27
Q

Regeneration Definition

A

Re-growth of axonal processes which reform along the same pathway and form the same (or similar [functional]) synapses as prior to damage

28
Q

Regenerative sprouts grow from…

A
  • cut axon
  • Sprouts may need to travel short or long distances through or around glial scar tissue
  • Either form new synapses on appropriate target tissue, form new synapses on inappropriate target tissue, or die.
29
Q

Regeneration mimics…

A
  • Mimics Embryonic Neural Migration

- Forward end of neural process (axon or dendrite) forms a growth cone

30
Q

When growth cone arrives at target cell

A

Synaptic vesicles form

Release of neurotransmitter stimulates postsynaptic membrane to develop receptor sites

31
Q

Regeneration in PNS

A

-the PNS of mammals, humans, and lower vertebrates do regenerate
-Regenerated axon has an inter-nodal length, axon diameter and conduction velocity that is 80% of normal
1 mm/month [Noback]
1-3 mm/month [NIH]

32
Q

Regeneration of PNS in humans

A
  • Schwann cells provide pathways (tunnels) that guide axons to regenerate along same path and reconnect properly
  • Form pathways across the scar tissue
  • Multiple axonal sprouts are generated and the sprout that reaches the target tissue survives (mimics development)
33
Q

Regeneration of CNS in humans

A

Oligodendroglia glial cells - apparently do not have the ability to line up as guiding tubes so that axons become entangled and/or scar tissue blocks CNS regeneration

Astrocytes – appear to block or inhibit regeneration

34
Q

Regenerative sprouting

A
  • Neural regeneration occurs most frequently in PNS bc Schwann cells produce nerve growth factor, which help recovery.
  • Astrocytes and microglia form glial scars, which physically block axonal regeneration
  • Oligodendrocytes produce Nogo (neurite outgrowth inhibitor) -> inhibits axonal regeneration
35
Q

Pharmacological approaches to enhance regeneration

A
  • NGF (nerve growth factor) - a high molecular weight protein that appears to be produced or taken up by nerve end feet and transported to the cell body
  • Possibly plays a role in maintaining normal growth or health of the cell
  • NGF appears to reduce scar tissue and enhance re-growth
36
Q

Remove scar tissue & suture nerve ends together to enhance regeneration

A
  • Difficult microscopic surgery
  • Cut the spinal cord and widened the gap (removed 5 mm of spinal cord) in rats to ensure that no tissue remained to produce false-positive results
  • High amount of inhibitory factor in white matter, but growth in gray matter relatively easy to stimulate
  • Surgeons carefully connected white matter to gray and gray matter to white
37
Q

Remove scar tissue & suture nerve ends together

A
  • used fibrin and fibroblast growth factor as a natural adhesive
  • nothing happened first 3 months
  • ~3 months, rat started flexing the hind limbs
  • at 1 year post, rats could support their weight, move their rear legs, BUT still not walking normally
  • probably very few axons crossing the gap, no more than 10%; this means we don’t have to re-grow the whole spinal cord to obtain significant function
38
Q

Nerve chambers that enhance regeneration

A
  • silicone tube implanted at the injury site
  • best recovery occurred when the tube was 2.5 x the diameter of the cut nerve
  • best recovery when the tube was thin walled but not so thin that it collapsed
  • adhesive matrix forms on the tube surface and guides the axons as they grow
39
Q

Nerve chambers recovery

A
  • small diameter axons (pain sensation & sweating) recovered to a greater degree than larger diameter MNs
  • methylprednisolone (MP) AND guidance tubes -> contained 4x more regenerated axons than tubes without MP
40
Q

Placement of undifferentiated or embryonic tissue enhance regeneration

A
  • Placement of undifferentiated or embryonic tissue in the path of re-growth to assist the guiding and regeneration across the area of scarring
  • Have had success in experimental animals
  • may provide a bridge across the scar tissue, a path to target tissue, & chemically stimulate re-growth
41
Q

Stem Cells

A
  • precursor or progenitor cells that have the potential to transform into a wide variety of tissue
  • As our CNS develops, embryonic stem cells evolve into more specialized adult neural stem cells.
  • these adult cells can differentiate into neuron- or glial-restricted precursor cells
  • -Neuron precursor cells-> neurons
  • -Glial precursor cells -> oligodendrocytes & astrocytes.
  • Given the wrong cues, stem cells can turn into physiological troublemakers -> cancer.
42
Q

Embryonic Stem Cells

A
  • after an egg is fertilized, an embryo is formed, which then splits into a two-cell embryo. This division goes on, successively creating 8, 16, 32, 64, 128-cell embryo
  • 4-6 days, the cells rearrange into 2 layers:
  • -Outer layer which will develop into placental and amniotic tissue
  • -Inner layer or a few dozen cells called the inner-cell mass (ICM) which turns into everything else.
  • -Now labeled a blastocyst, the embryo is about 0.1-mm across or the size of the period at the end of this sentence.
43
Q

Blastocyst & Inner Cell Mass

A
  • After about 2 weeks, the ICM cells start to organize into 3 specific layers that become our various tissues.
  • -Ectoderm
  • -Mesoderm
  • -Endoderm

-As the cells continue to develop, they increasingly lose their omnipotent nature

44
Q

Embryonic Stage (2-8 weeks): Ectoderm develops into…

A

Sensory organs
Epidermis
Nervous system

45
Q

Embryonic Stage (2-8 weeks): Mesoderm develops into…

A

Dermis
Muscles
Skeleton
Excretory and circulatory systems

46
Q

Embryonic Stage (2-8 weeks): Endoderm develops into…

A

Gut, liver, pancreas

Respiratory system

47
Q

To obtain embryonic stem cells…

A

-ICM cells are isolated before they start turning into these layers, and are grown in culture

48
Q

Cell Sources

A
  1. Embryonic Stem Cells – IVF Clinics
  2. Fetal Stem Cells
  3. Adult Stem Cells (Bone Marrow, Blood, etc.)
  4. Umbilical Stem Cells (umbilical cord blood, etc.)
49
Q

Olfactory-Related Programs

A
  • Carlos Lima (Portugal), olfactory tissue, OMA (olfactory mucosa autograft)
  • Because olfactory tissue is exposed to the air we breathe, it contains cells with considerable turnover potential, including renewable neurons, progenitor stem cells, & olfactory ensheathing cells (OECs) NASAL MUCOSA
  • When transplanted into the injured spinal cord, OECs potentially promote axonal regeneration by producing insulating myelin sheaths around both growing & damaged axons, secreting growth factors, & generating structural & matrix macromolecules that lay the tracks for axonal elongation

Neuro Science (10 decks)

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