NeuroPlasticity Flashcards
Neuropraxia
Local myelin damage, axon remains intact
Axonotmesis
Usually bounce back
Continuity of axon is lost
May or may not include damage to epineurium, perineurium, and/or endoneurium
Loss of continuity leads to Wallerian degeneration - after the point of injury everything distal degenerates
Neurotmesis
usually can’t grow brack require surgery
Complete transection of nerve
cellular events after a peripheral nerve injury
Wallerian degeneration – everything after injury dies
Macrophages begin to clear debris AND Schwann cells become phagocytic and engulf degenerating axon and myelin
Central end of axon sprouts into endoneurial sheaths left behind by degenerated axon
Schwann cells proliferate as axon regrows
Production of new myelin
Guide axonal regrowth
Axon re-establishes postsynaptic target
Axon diameter increases, more myelin created with time
Axonal sprouting
collateral vs regenerative
Regenerative is where you take the normal events of a peripheral nerve injury
collateral sprouting is where neighboring nerve receptor sprouts and hits nerves close by of the one that died can no longer reach
3 causes of axonal injury
trauma
ischemia
neurodegenerative disease
Bad news and good news for CNS
THE BAD NEWS:
CNS axons typically do not re-grow after injury
THE GOOD NEWS:
Our brain has an incredible capacity to create new pathways to compensate for the axons lost
Why doesn’t the CNS regen
CNS damage “triggers” necrosis and apoptotic cell death of severed axons
Clean up is slow
- no schwann cell
- no macrophages
CNS environment is hostile to regenerative attempts
- astrocytes cause glial scarring
- microglial activation - gets rid of bad and good stuff
Neurogensis
The creation of CNS neuronal growth
there is a low level of glial cell proliferation
2 areas of our brain that show potential for neurogenesis
olfactory bulb
hippocampus
Neuroplasticity
The ability of the nervous system to respond to intrinsic stimuli by reorganizing its structure, function and connections
Neuroplasticity mechanisms
chemical
structural
functional
differences between chemical, structural, functional mechanisms
chem - immediate or short-term
Structural - long-term changes to neuronal structure
functional - long-term changes to the neuronal function
somatotopic organization of Pre and Post central gyrus
middle is legs
outside is face
Habituation
simplest form of neuroplasticity
decrease in response to a repeated stim
ex: people that can sleep in the city get used to car sounds
short term habituation
less than 30 mins
Changes pre-synaptically
↓ release of excitatory neurotransmitters
Effects are transient
long-term habituation
more than 30
Changes post-synaptically
↓ receptors on postsynaptic receptors
Learning and memory
Is manifested through long-term potentiation and depression
long-term potentiation receptors
post synaptic receptors
AMPA
NMDA
AMPA permeable to and receptor type
Na+
glutamate receptor
NMDA permeable and special?
Ca and Na
contain Mg2 blockade in channel
how does electrostatic repulsion work
Mg2 gets pushed out by a higher action potential - from the influx of Na - and then more Na and Ca can get in the postsynaptic neuron
NMDA call coincidence receptors
because they need specific pre and postsynaptic events to occur
What changes in the post synaptic neuron with calcium
↑ postsynaptic AMPA receptors
↑ growth factors -> new synapses
what does calcium do in presynaptic neuron
exocytosis
Long term depression
Reset button
caused by low intensity prolonged stimulation
Rehabilitation and neuroplasticity
tech
pharm - fluoxetine
cognitive
physical rehab
10 principles
use it or lose it use it or improve it specificity matters repetition intensity Time salience age transference interference
