Neuroplasticity Flashcards
(30 cards)
Molecular level neuroplasticity
upregulation of proteins
gene expression
Single neuron level
synaptic plasticity
Network level
cortical maps
Systems level
within and across systems of CNS
Principles of Training
many reps
progressive level of challenge
allow for success most of time/some failure
motivation/reward/meaningful goals
Other considerations for learning
sleep - consolidation of memories
rest periods - incorporation of memories
limit interference
Synaptic plasticity - increase in motor cortex; when?
dendritic branching, spine density
perforated synapses
synapses with multiple synaptic boutons
after environmental enrichment or learning of specific motor tasks
Synaptic plasticity mechanisms
synaptic activity (2nd messenger systems) –> enzyme activation –> gene expression –> protein synthesis –> cell changes
Synaptic plasticity - cell changes
dendritic branching synaptogenesis collateral growh neurotransmitter receptor
Synaptic plasticity - ST changes
min to hrs
upregulation of NTs/receptors
protein synthesis increases
Synaptic plasticity - LT changes/potentiation
days or longer
collateral growth
spine and synapse formation
potentiation - less input needed to generate same output = learning
Timeline with Skill Training
7 days - synapse
10 days - maps
within minutes - protein synthesis
Endurance Training
angiogenesis in M1
reduce motor thresholds in SC
NO change in motor map
Lesion
recovery of function –> minimizing impairment
OR
compensation –> adaptation to impairment
Phase of Recovery: Rescue and Salvage
few hours - tPA, neuroprotection
neural shock
penumbra
Phase of Recovery: Repair and Recovery
days to weeks to months
behavioral and pharmalogical
max adaptive plasticity
Vicariation of Function (adaptive plasticity): distribution of motor cortex changes
changes in motor maps
competitive process
use dependent plasticity
Vicariation of Function (adaptive plasticity): growth of novel circuits
new pathways formed
circuitry of brain changes
Secondary cell death
excitotoxicity
formation of O2 free radicals
2ndary ischemic damage
Diaschisis
inhibition of neurons related to damaged area (due to neural shock, edema, loss of blood flow, partial denervation)
more likely to happen with sudden insult
reversible
Wallerian Degeneration
primary damage
Transneuronal Changes
increased synaptic efficiency of remaining synapses
denervation supersensitivity - receptor upregulation
unmasking of silent synapses
collateral sprouting from adjacent neurons
TMS
transcranial magnetic stimulation
used in humans to measure changes in cortical motor maps
induce ion flow across membranes of cortical neuron (ion exchange causes APs to generate)
Aging Machinery
decline in function seen with aging is inevitable and irreversible
