Term
| What does neural plasticity enable? |
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Definition
Development of functional connections
Learning, Creativity, Memory
Day-to-Day functions
Fine Tuning Performance
Repairing Neural Damage |
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Term
| Why will death result from no plasticity? |
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Definition
| A lot of synapses are first made incorrectly. Must be refined/eliminated. |
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Term
| Describe synapse elimination during development of a rat eye. |
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Definition
| Newborn rats have diffuse connections to SC spread out throughout the retina, but go retina (Nasal-temporal) to SC (Caudal-anterior) as different brances are retracted, completed when eyes open, but started well before. |
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Term
| What is the underlying basis for Hebb's hypothesis? |
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Definition
| neurons compete for a limited supply of growth factors. |
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Term
| What are some common trophic factors? What do they do? |
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Definition
NGF (nerve growth factor)
BDGF
FGF
CNTF
Not food, necessary for maintenance and growth of axon terminals, and synapse maintenance |
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Term
| How do trophic factors migrate to where they are utilized? |
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Definition
1. Growth factors taken up at axon terminal
2. Transported retrograde to soma
3. initiates a cascade |
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Term
| What is the modern understanding of Hebb's Hypothesis? |
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Definition
| trophic factors are released from post-synaptic cells in proportion to the amount of depolarization it undergoes, but the trophic factors can only be take up and utilized by simultaneously active pre-synaptic terminals. |
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Term
| What are some principles of Hebbian Plasticity? |
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Definition
More post-synaptic stimulation -> more trophic factors released
More active pre-synaptic cell -> better uptake of trophics
More trophic factor uptake -> bigger terminal + boutons
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Term
| What is long-term potentiation (LTP)? |
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Definition
A long term increase (hours-weeks) in synaptic strength
Requires High Frequency theta waves (50-100hz)
Large fast changes in Calcium concentration
Protein sysntehsis increases synaptic efficacy |
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Term
| What is long term depression? |
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Definition
Long-term decrease in synaptic strength.
Requires prolonged low frequency (1hz, 1000 pulses) stim
Small, slow change in Calcium
Protein synthesis decrease synaptic efficacy |
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Term
| What kind of cells has LTP been studied in? |
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Definition
| Shaffer collaterals in the hippocampus. |
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Term
| Describe the early phase of LTP in Shaffer Collaterals |
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Definition
increased neurotransmitter release, increases sensitivity
lasts 1-3 hours, doesn't require protein synthesis. |
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Term
| Describe the late phase of LTP in Shaffer collaterals. |
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Definition
Lasts at least 24 hours
New boutons are formed
Requires protein synthesis
Uses the cAMP-PKA-MAPK-CREB pathway |
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Term
| What is implied by Hebbian activity? |
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Definition
Neuronal activity is essential for refinement
More boutons, more likely maintained connection
Synchronous activity is neccessary |
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Term
| How is retinotopy induced by hebbian conditioning? |
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Definition
| spontaneous activity in the retina before eyes open group close cells together -> spatial map |
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Term
| What happens when there isn't enough stimulation of a neuron? |
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Definition
Neuron retracts synaptic terminals and dies
Trophic factors prevent activation of endonucleases (degrades DNA) and caspases (degrades protein)
Apoptosis |
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Term
| What are sensitivity periods? |
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Definition
| periods in development when the capacity for adjustment in response ot experience is much greater than in adulthood |
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Term
| What is a critical period? |
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Definition
| period of development that requires appropriate input for the correct formation of a set of connections. |
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Term
| How can binoccular vision be affected by a critical period? |
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Definition
Combining inputs from both eyes requires normal binoccular vision in early life, with good alignment and good optics in both eyes
Amblyopia results from bad eye alignment or poor input during the critical period; the brain suppresses weak information.
Studied in cats (critical period <3months old)
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Term
| What is the implication of loosing an eye after reaching adulthood on steropsis? |
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Definition
| None, you can keep stereopsis |
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Term
| What happens to occular dominance columns if cats are monoccularly deprived early in life during the critical period? |
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Definition
| Much larger numbers of monoccular cells in V1, thins out the size of the occular columns. |
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Term
| How can occular dominance plasticity be restored in adult animals? |
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Definition
| Suppress the inhibition mechanisms, prevent the brain from becoming silent, leads to hallucinations. |
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Term
| How is motor learning associated with neural plasticity? |
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Definition
Motor skill learning is associated with creation of new synapses, through reorganization
Finger Map expands as training increases
Motor skill learning requires protein syntehsis after training |
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Term
| What are some common ways to tell if cortex is reorganized? |
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Definition
changing receptive fields.
Microstimulation can induce plasticity in somatosensory (honed in on receptive field) and visual cortex (change orientation pinwheel) |
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Term
| What are some influences on learning a motor skill effectively? |
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Definition
task difficulty
Motivation
Arousal
Reward/Punishment
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Term
| What are the three proposed mechanisms of perceptual learning in the brain? |
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Definition
Hebbian Reweighing
Reverse Hierarchy
Rule-based |
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Term
| Describe the reverse hierarchy model. |
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Definition
Lower hierarchy levels feed forward small discrete receptive fields
Higher levels feedback details about the big picture (scrutiny) |
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Term
| What do you need to repair the brain and recover functionality? |
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Definition
1. Replace lost neurons
2. Re-grow lost connections
3. Retrain new/alternative circuits to perform lost functions |
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Term
| What are some diffuse types of injury to the brain? |
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Definition
| Neurodegenerative disease (parkinsons, Lou Gehrigs) |
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Term
| What are some focal injuries to the brain? |
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Definition
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Term
| Do neurons always die when they are injured? How many neurons can be lost before you can lose function significantly? |
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Definition
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Term
| What does injury do to supporting cells of neurons (glia) |
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Definition
Glial death
Reactive Gliosis
Glial Scarring |
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Term
| What happens to neurons deprived of their target? |
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Definition
Depends if they are connected to only one target or many.
One target -> Death due to lack of trophic factors
Multi-target -> probably ok, just lose a branch |
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Term
| What happens to neurons deprived of their stimulating input? |
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Definition
Like development
Diffuse spontaneous activity
Lack of activity -> harder to compete for targets upstream |
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Term
| How can we replace neurons? |
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Definition
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Term
| Why is using neurogensis to replace neurons hard? |
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Definition
doesn't normally occur in adult cerebral cortex, aside from hippocampus
can be modulated by age (less), stress (less), exercise (more), and learning (more) |
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Term
| Where do adult neuron progenitors go following a brain lesion? |
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Definition
| they migrate toward the lesion site for a short time, even if in cortex. |
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Term
| What are some problems associated with re-growing lost cortical connections? |
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Definition
Myelin and oligodendrocytes doesn't allow outgrowth
glial scarring doesn't allow growth
no more chemotaxic clues to guide growth |
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Term
| How can neurons re-grow some lost connections? |
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Definition
horizontal growth of connections in cortex
young neurons can grow through adult cortex and white matter.
block myelin production (NoGo receptors blocked) |
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Term
| How can we retrain the damaged adult circuits to perform new functions? |
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Definition
Works in motor cortex after injury, by forcing use of damaged hand, reorganizes receptive fields
Works in visual cortex, train amblyopes to pay attention to their bad eye.
somewhat controversial studies, poorly controlled |
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Term
| How did Huxlin et al retrain some visual cortex damage? |
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Definition
Used connections from LGN to MT, instead of the normal visual pathway
Practiced with motion discrimination in bad fields of view, reactivates good parts of V1 and higher levels through reciprocal connections (retinotopic)
Increased the good amount of visual field stimuli, improves other motion perceptions |
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