Neuroplasticity Flashcards
What is neuroplasticity?
potential for brain to reorganise with new neural pathways to change/adapt
single neuron to whole brain cortical remapping
brain function can change in response to experience/training
how does brain volume change during development
initial growth gray matter in cortex = start in primary sensory + motor regions then gradual decline (esp in higher order association area)
white matter increases throughout early childhood + adolescence
what is meant by ‘types of synapses change’
ratio of excitatory to inhibitory synapses change, particularly in prefrontal cortex
more inhib as oler
compare % of axon in fetal primate brain v adult brain
30-60% more fetal
corpus callosum has 400% more
how does synaptic pruning occur (directionally)
gradually prund away
caudal-rostral direction following birth > continues into young adulthood
avg adult = 8000 connections
50% lost during adolescence due to competitive eliminiation
Role of microglia in synaptic pruning
microglia monitor + interact with synapses => modulate circuit formation = function
phagocytose weak synapses during development/injury
impac of pruning on dendritic spine density
rapid spinogenesis post-natally, then pruning in adolescence
equilibrium in adulthood, some spines constantly added/remove
what happens with fragile x syndrome
region on long arm of x chromosom = fragile bc unstable DNA
>CGG repeats
abnormal facial apperance, mild-sevre cog impairment
excess smal, immature dendritic spines on cortical neurons, due to loss of normal synaptic pruning
how does brain choose which synapses to eliminate
cell that fire together, wire together
synchony causes firing in post synaptic neuron
ones that are not causing firing = flagged for pruning
role of neurotrophic factors
active synapses take up neurotrophic factor, maintains synapse
what is a strengthened synapse - ltp
over time, stim causes greater responses
dependent on presynaptic glutamate release (bind to NMDA + AMPA on post)
EPSP unblocks NMDA mg2+ from NMDA receptor for in rush of CA2
=> trigger 2nd msngr for inc post synap AMPA insertion
what are the lasting changes with ltp
ca2+ influ activates kinases = acts on substrates to induce local change eg alter morphology/transcription of RNA
mRNA translated into proteins = stabilise synaptic change
what is the critical period
time when experience most counts
once it ends, core features of behaviours are largely unaffcted by subsequent experience
failure to be exposed to appropriate stimuli may be difficult to remedy later
examples of critical period
some behaviour pressed only if animal has specific experiences during specific window of time after birth
others = detailed instructive experiences from env (learned from tutor birds)
hubel + wiesel = visual cortical neurons divided into ocular dominance
usually normal distribution, but suture eye of kitten => functional disconnection where open eye rives almost all cell
=> amblyopia = permanent
adult eye close? function is relatively normal
what happens in the brain with ocular dominance?
alternating ide trips in macaque brain
after deprivation: non deprived eye whitestripes = wider,
deprived eye black trip = shrunken
inputs from active ye take over territory = competitive interaction
