Neuroplasticity Flashcards
what is the hebbian plasticity theory
neurons that fire together, wire together
- # more connections and APs that are sent = stronger connection
- less firing = weaker connection
what does plasticity signify
learning is taking place
what is unimodal plasticity
synaptic plasticity through experience (ex: learning braille) can lead to growth of specific portions of the body map in S1
what is cross modal plasticity
strengthening of somatosensory and auditory cortex input through LTP due to blindness or other loss of sense
ex: through congential blindness - cross modal more prevalent in people who were blind early in life
what causes LTD
low frequency stimulation (< 1Hz) applied to schaffer collaterals
small, slow rises in post synaptic calcium leads to LTD
what happens during LTD
opposite of LTP - removal of AMPA receptors and shrinking / eventual removal of the synapse / dendrite
why is LTD necessary
needed to prune out neurons not following Hebb’s law
(not being used / stimulated so connection weakens)
what are place cells
fire APs when they are in a particular location within their environment
(used to recognise places)
where are place cells found
posterior hippocampus
(can experience anatomical changes (growth) as people learn more places)
what is the dentate gyrus
one of the only locations in the brain where the birth of new neurons occurs (neurogenesis)
why does neurogenesis occur in the dentate gyrus
constantly experiencing new places so new place cells are needed
what is the difference between specificity and associativity
specificity = LTP is specific to one synapse when the other is inactive
associativity = strong stimulation can cause growth (LTP) at a pathway with weak stimulation
how does a bicep curl represent associativity
both biceps and triceps fire - even though triceps have a weak stimulation there would be no movement without them
during LTP, why do EPSPs increase and then decrease back to baseline
LTP causes dendritic spines to grow
- growth = more ions flowing in but increased SA means its more leaky
- leakiness causes EPSPs to return to baseline
what does the morphology of dendritic spines determine
their electrical properties which can have direct effects on EPSP/IPSP amplitudes
what does repeated activation of post synaptic neuron cause
additional AMPA (glutamate) receptors are inserted into the post synaptic membrane
which receptor(s) does glutamate bind to
both AMPA and NDMA receptors
which receptor does glutamate activate and which ion is allowed to flow
activates AMPA
sodium flows (only ion flow at the beginning of EPSP)
what does sodium flow through AMPA lead to
makes post synaptic potential more positive leading to an EPSP
what is the effect of an EPSP on NDMA
magnesium blocker on NDMA is repelled by EPSP and both sodium and calcium and flow through
what are CaMKII and PKC
calcium activated protein kinases (enzymes)
calcium binds to these enzymes to initiate the process of LTP (more AMPA receptors added to post synaptic neuron)
- blocking these enzymes stops LTP
what are the two phases of LTP
- AMPA receptors inserted into post synaptic membrane
- growth of dendritic spines is stimulated
what are the pros and cons of dendritic spines
pro = reduces axoplasmic resistance in the dendrite (easier for ions to flow from the head to the dendrite)
con = increases SA (more room for ions to leak out)
what are the basic steps that lead to LTP (6)
- glutamate binds to AMPA
- sodium only flows through (makes more positive)
- EPSP caused
- NDMA magnesium blocker repelled by EPSP
- sodium and calcium flow occurs
- more AMPA receptors added as communication continues
what is the initial benefit of more AMPA receptors during LTP
leads to larger EPSPs (easier to achieve / more sensitive)
more channels to let sodium in