Ch. 4: Neuroplasticity Flashcards
Signs/Sx of Nerve Irritation
Tingling
Signs/Sx of Asleep Nerve
Sensation/Motor Loss
Signs/Sx of Nerve Death
Sensation/Motor Loss
Wallerian Effect
Distal to axon injury
Habituation
- decrease strength of synaptic connections (like down regulation)
- Short-lived decrease in strength of response following repeated benign stimulation
- May be due to decrease release of excitatory neurotransmitters
Adaptation
-Structural changes due to long term habituation
LTP
- Long term potentiation
- Persistent, long lasting changes in strength of synaptic connections
-AKA: experience-dependent plasticity
Conversion of Silent Synapses to Active Synapses
- AMPA Receptors inside post synaptic cell get pushed to the membrane for use when Calcium enters the cell though other (NMDA) receptors when glutamate binds to it
- with stimulation: post synaptic cell creates another dentritic spine with clusters of receptors and presynaptic membrane changes shape too
Types of Sprouting
- Regenerative
- Collateral
Regenerative Sprouting
-Damaged neuron regrows axon if soma still alive
Retrograde Effect
-Proximal to axon injury
Stroke (FAST)
F-facial droop
A-arm weakness
S-slurred speech
T-time
Recovery of synaptic effectiveness
- Resolution of swelling–>axon wakes up
- “shadow of death” recovers and regains blood supply
Collateral Sprouting
- if soma dies after injury a surviving neuron sends out a branch to the target cell
- Collaterals can fail over time
Axonal Injury in CNS
Doesn’t sprout collaterals or regenerate
CNS MOI
- Mechanical (tear, shear, projectile)
- Chemical (ischemia, excitotoxicity)
Synaptic Hypereffectiveness
- Divergent nerve partially damaged but still produce same amount of neurotransmitters
- the remaining terminals release all the NT in attempt to still send messages
Unmasking of Silent Synapses
- (long term potentiation)
- creates new neural pathways by stimulating a synapse to put receptors on the membrane
4 Synaptic Changes after CNS injury
- recovery of synaptic effectiveness
- denervation hypersensitivity
- synaptic hypereffectiveness
- unmasking silent synapses
Denervation Hypersensitivity
- upregulation of receptors on post synaptic membrane
- Nerves down stream of injury insert more receptors to try to re-establish message
- bad if random NT comes by and inappropriately signals neurons
Metabolic Effects of Brain Injury
- large quantiy of glutamate released from dead/oxygen deprived nerves
- glutamate binds to NMDA receptors
- too much calcium into cell–>excitotoxicity
Plasticity
- Change in # of connections
- change in strength of connections
Experience-Dependent Plasticity
- basis of learning and memory
- turn up strength of synaptic connections (via up regulation)
- aka Long Term Potentiation
Mechanism of LTP
- Conversion of silent synapses to active synapses
- change morphology of pre and post synaptic membranes
Astrocytes in LTP
- Store and release calcium (for remodeling)
- release glutamate (instigator of remodeling)
- modulate NT release and receptor expression (via Calcium) on post synaptic membrane
Initial Response to Peripheral Axon Injury
- Retraction of Proximal Segment
- Degeneration Distal Segment
- Chromatolysis in Cell
- Effects on Postsynaptic Membrane
Too much calcium in the cell–>
- decreases pH and break down membrane
- proteases break down cell proteins
- Oxygen free radicals decrease mitochondria function
- increase solute concentration in cell and water follow and cause swelling
