neuroplasticity Flashcards

1
Q

what is plasticity?

A

capacity for neuronal change

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2
Q

4 main neuroplastic responses?

A

1) degeneration
2) regeneration
3) reorganisation
4) recovery

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3
Q

neural degeneration: types

A
  • Anterograde deterioration: deg of the distal segment (by synaptic terminals) (quicker)
  • Retrograde deterioration: deg of the proximal segment (closer to cell body) (gradual)
  • transneuronal degeneration: when degeneration spreads to neurons linked via synapses
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4
Q

retrograde deterioration can change the cell body

A

Can be:
Degenerative –> decrease in size leading to autopsis
Regenerative –> increase in size indicates that the cell body is making proteins to replace those lost in degen BUT DOESNT mean it’ll SURVIVE

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5
Q

types of transneuronal degeneration

A
  • Anterograde transneuronal degen: when degen spreads from damaged neuron to neuron ON WHICH they synapse:
  • Retrograde TND: spreads to neurons that synapse ON THEM
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6
Q

where is neuronal regeneration virtually non existent?

A

CNS

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7
Q

axon regrowth can occur in 3 different ways

A

1) schwann cell guidance
2) medium sized gap between the halves
3) overly large gap between the halves

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8
Q

axon growth in PNS using Schwann cells in small gap

A

if original schwann cells are intact, the axon will grow through the original sheath to their correct/ORIGINAL targets

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9
Q

axon growth in PNS when the gap is mediocre in size

A

the axons may end up reforming and connecting with the wrong alternate half (incorrect axons –> incorrect sheath –> incorrect destination)

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10
Q

axon regeneration in PNS when the gap is widely separated

A

the axons may become tangled around the proximal stump & die

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11
Q

what is it in the PNS system that allows the axons to regenerate?

A

Schwann cells (only in PNS)

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12
Q

Purpose of schwann cells

A

clear debris resulting from degeneration & promote regeneration

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13
Q

how do schwann cells promote regeneration?

A
  • neurotrophic factors: proteins released that stimulate growth of axons
  • Cell adhesion molecules: mark the paths that the PNS axons can take to grow
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14
Q

CNS equivalent to PNS schwann cells?

A

Oligodendroglia (aka oligodendrocytes)

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15
Q

what do oligodendroglia do?

A
  • actively block regeneration (Yiu & He 2006)

- survive much longer after the nerve damage (Vargas & Barres, 2004)

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16
Q

what is the function of oligodendroglia? (2)

A

1) support & insulate axons in CNS

2) create the myelin sheath - essential for control & electrical charge

17
Q

collateral sprouting - what?

A
  • when axons grow out from healthy neurons & take up the now empty sites of degenerated neurons
  • can grow out from terminals & nodes of ranvier
18
Q

mechanisms of neural reorganisation (5)

A

1) strengthening of existing connections through release of inhibition
2) collateral sprouting
3) adjustment of dendritic trees
4) adult neurogenisis
5) training in non- affected area

19
Q

neural reorganisation –> strengthening of existing connections through release of inhibition

A

evidence in support:

  • reorganisation occurs too quickly to be explained by neural growth
  • rapid reorganisation never covers extensive surface
20
Q

neural reorganisation –> collateral sprouting

A

evidence in support:

- magnitude of long term reorganisation is too great to be explained by strengthening of current neurons

21
Q

neural reorganisation –> adjustment of dendritic trees

A

make more links & connections (Wilson, 2007)

22
Q

neural reorganisation –>adult neurogenisis

A
  • process of generating new neurons which integrate into existing circuits as an adult
  • only really occurs in olfactory bulb & hippocampus
23
Q

neural reorganisation –> training

A

Nudo (2013)

- training will help functions to return

24
Q

recovery of function is hard to study bc there are other compensatory mechanisms which may be confused with plasticity (3)

A

1) cerebral edema: swelling in brain; if reduces in a few week may seem like recovery of function
2) learning of new cog & beh strategies: may dev new ways to do a task; subst of function > return of lost function
3) cognitive reserve: intelligence & education

25
Q

neuroplastic responses to recovery

A

1) Nishimura et al. (2007) show that neurop changes to undamaged areas have contributed to recovery after CNS damage
2) adult neurogenesis (Zhal et al. 2003) & stem cell creation in hippocampus
~~~BUT isnt evidence to support the long distance travelling of stem cells

26
Q

treatment of neuronal damage: 4

A

1) promoting regeneration
2) blocking neurodegeneration
3) neurotransplantation
4) rehabilitation

27
Q

promoting regeneration

A

a) eliminate inhibition from oligodendroglia
b) provide schwann cells to direct growth (Cheng, cao & olsen 2006)
c) transplanting olfactory ensheathing cells (raisman & Li 2007)

28
Q

blocking neurodegeneration

A

a) autopsis inhibitor protein
b) nerve growth factor: promotes growth over degeneration (sofroniew et al. 2001)
c) estrogens: limit death & decay

29
Q

neurotransplantation

A

a) FETAL TISSUE: big debate on use (dunnett, Bjorklund & Lindrall 2001)
b) STEM CELLS: mulitpotent
more research needed (Li et al. 2008)

30
Q

rehabilitation

A
  • constraint induced therapy ( Taub et al 2002)

- facilitated walking to treat spinal injury (wolpaw & Tennissen 2001)