neuroplasticity Flashcards
what is plasticity?
capacity for neuronal change
4 main neuroplastic responses?
1) degeneration
2) regeneration
3) reorganisation
4) recovery
neural degeneration: types
- 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
retrograde deterioration can change the cell body
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
types of transneuronal degeneration
- Anterograde transneuronal degen: when degen spreads from damaged neuron to neuron ON WHICH they synapse:
- Retrograde TND: spreads to neurons that synapse ON THEM
where is neuronal regeneration virtually non existent?
CNS
axon regrowth can occur in 3 different ways
1) schwann cell guidance
2) medium sized gap between the halves
3) overly large gap between the halves
axon growth in PNS using Schwann cells in small gap
if original schwann cells are intact, the axon will grow through the original sheath to their correct/ORIGINAL targets
axon growth in PNS when the gap is mediocre in size
the axons may end up reforming and connecting with the wrong alternate half (incorrect axons –> incorrect sheath –> incorrect destination)
axon regeneration in PNS when the gap is widely separated
the axons may become tangled around the proximal stump & die
what is it in the PNS system that allows the axons to regenerate?
Schwann cells (only in PNS)
Purpose of schwann cells
clear debris resulting from degeneration & promote regeneration
how do schwann cells promote regeneration?
- neurotrophic factors: proteins released that stimulate growth of axons
- Cell adhesion molecules: mark the paths that the PNS axons can take to grow
CNS equivalent to PNS schwann cells?
Oligodendroglia (aka oligodendrocytes)
what do oligodendroglia do?
- actively block regeneration (Yiu & He 2006)
- survive much longer after the nerve damage (Vargas & Barres, 2004)
what is the function of oligodendroglia? (2)
1) support & insulate axons in CNS
2) create the myelin sheath - essential for control & electrical charge
collateral sprouting - what?
- when axons grow out from healthy neurons & take up the now empty sites of degenerated neurons
- can grow out from terminals & nodes of ranvier
mechanisms of neural reorganisation (5)
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
neural reorganisation –> strengthening of existing connections through release of inhibition
evidence in support:
- reorganisation occurs too quickly to be explained by neural growth
- rapid reorganisation never covers extensive surface
neural reorganisation –> collateral sprouting
evidence in support:
- magnitude of long term reorganisation is too great to be explained by strengthening of current neurons
neural reorganisation –> adjustment of dendritic trees
make more links & connections (Wilson, 2007)
neural reorganisation –>adult neurogenisis
- process of generating new neurons which integrate into existing circuits as an adult
- only really occurs in olfactory bulb & hippocampus
neural reorganisation –> training
Nudo (2013)
- training will help functions to return
recovery of function is hard to study bc there are other compensatory mechanisms which may be confused with plasticity (3)
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
neuroplastic responses to recovery
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
treatment of neuronal damage: 4
1) promoting regeneration
2) blocking neurodegeneration
3) neurotransplantation
4) rehabilitation
promoting regeneration
a) eliminate inhibition from oligodendroglia
b) provide schwann cells to direct growth (Cheng, cao & olsen 2006)
c) transplanting olfactory ensheathing cells (raisman & Li 2007)
blocking neurodegeneration
a) autopsis inhibitor protein
b) nerve growth factor: promotes growth over degeneration (sofroniew et al. 2001)
c) estrogens: limit death & decay
neurotransplantation
a) FETAL TISSUE: big debate on use (dunnett, Bjorklund & Lindrall 2001)
b) STEM CELLS: mulitpotent
more research needed (Li et al. 2008)
rehabilitation
- constraint induced therapy ( Taub et al 2002)
- facilitated walking to treat spinal injury (wolpaw & Tennissen 2001)
