Neuroplasticity Flashcards
Term: The ability of neurons to change their functions, chemical profile, or structure for longer than a few seconds
Neuroplasticity
3 Mechanisms of Neurplasticity
- Habituation
- Experience-dependent plasticity
- Recovery following injury
Term: Decrease in response to a repeated, benign stimulus due to a decrease in synaptic activity between sensory neurons and interneurons
Habituation
Describe the effect of absence of the stimulus on habituation
After a period where the stimulus is not applied, the effect resolve or diminish, once the stimulus is reapplied the response will return
Describe the effects of prolonged, repeated stimulus on habituation
Can result in more permanent, structural changes – the number of synaptic connections decreases
Term: Allows other types of learning to occur by letting people pay attention to important stimulation but “tune out” stimulation that is less important
Habituation
Term: Involved with learning and memory
Exeperience-dependent plasticity
Term: Persistent, long-lasting changes in the strength of synaptic connections between neurons and within neural networks
Exeperience-dependent plasticity
Describe the mechanisms behind Experience-dependent plasticity
- synthesis of new proteins
- growth of new synaptic connections
- modification of existing synapses
2 types of Experience-dependent plasticity
- long-term potentiation (LTP)
- long-term depression (LTD)
Describe how presynaptic and postsynaptic sysnapses change with Experience-dependent plasticity
Pre: through changes in NT release
Post: through changes in receptor density/efficiency
Term: “What fires together wires together”
LTP
Term: Prolonged stimulus results in growth of new cells/synapses
LTP
Term: Receptors englufed resulting in the synapses becoming inactive
LTD
Describe the role of astrocytes in Experience-dependent plasticity
Astrocytes modulate NT release and receptor expression at the post-synaptic membrance via the release of gliotransmitters, they may also be responsible for new synapse formation
Term: Remembering the 3 things you need to pick up at the store
Working memory
Term: Remembering a new phone number 5-10 minutes later
Short-term memory
Term: Recall of facts
Long-term memory – Delcarative – Semantic
Term: Recall of events
Long term memory – Declarative – Episodic
Term: Recall of facts and events
Delcarative Memory
Term: Recall of motor skills
Non-declarative – Procedural memory
Describe what an injury to an axon in the PNS looks like physiologically
- cytoplasm leaks out
- segments retract from one another
- distal Wallerian degeneration
- glia clean up debris
- cell body undergoes central chromatolysis
- potential synapse degeneration and death
Term: degeneration of axon and myelin distally along with mm atrophy
Wallerian degeneration
Term: cell body degenerative changes
Central chromatolysis
Describe regeneration of axons in the PNS
Regeneration occurs in the form of sprouting of damaged axons which is guided by nerve growth factor produced by Schwann cells and by Bands of Bungner
Recover is slow – 1 mm/day, but can be stimulated by exercise
Term: maladaptive rewiring; either alterned/crossed sensations or mm co-contraction
Synkinesis
Describe the post injury response in the CNS
The majority of the damage takes hours to days to evolve due to the cascade of cellular events which is why it can take time to see how a pt. will present
- white fiber tract damage leads to increased Ca influx
- leads to the disruption of axonal transport and results in build up
- leads to axonal swelling
- leads to axonal retraction ball
- leads to chromatolysis and Wallerian degeneration
Describe the difference between the physiology behind SCI and TBI
SCI: extent of deficit depends on damage of white tracts and level
TBI: interial forces can cause widespread tearing and stretching which can cause diffuse axonal injury (stretched/torn fibers) and widespread neuron disconnect
Describe the ability of the CNS to recover
Doesn’t occur as well as in the PNS
Regeneration is limited by glial scars which release neurite outgrowth inhibitor (Nogo)
2 Promising tx for CNS axonal injury
- Drugs to inhibit Nogo
- Stem cells
4 CNS synaptic changes following injury
- Recovery of synpatic effectiveness
- Denervation hypersensitivity (increase in receptors)
- Synaptic hypereffectiveness (increase NT release)
- Unmasking/disinhibition of silent synapses
Describe Cortical Reorganization
Cortical represenation can be modified by sensory input/experience/learning/injury. Performing a motor skill task regularly can enlarge that area of cortical representation
Describe the impact of genetics on cortical reorganization
Those with a BDNF gene have a decreased ability to learn a motor task and had poorer recovery following subarachnoid hemorrhages
The implications for PT include: could help direct plan to accomodation or rehabiliation, could also limit the pt. potential due to a stigma of inability to improve
2 areas in the adult brain where new neurons are produced
Hippocampus and the wall of the lateral ventricles
Describe the issue with naturally occuring neurogenesis
The new neurons/stem cells produced in the brain move to the area of injury but do not survive long enough to resolve the problem
Describe how rehabilitation can promote plasticity
- Intensity (too much to soon can be damaging)
- Type (task specific!)
- Amount (early and frequent)
