LTP and LTD Flashcards
synaptic plasticity
ability of synapses to strengthen or weaken over time. It is a history dependent change in synaptic transmission.
ways of distinguishing plasticity
potentiation/depression
time course (short/long)
where does synaptic plasticity occur
all regions of the brain (&SC)
how can synaptic transmission be measured
brain slices
in vivo
what induces synaptic plasticity
high/low frequency stimulation
different forms of synaptic plasticity
STP - over time dissipates
LTP - remains elevated, higher frequency
LTD
examples of short term plasticity
paired-pulse facilitation (PPF) pre synaptic plasticity
post-tetanic potentiation (PTP)
LTP duration
very long lasting (1 year recording)
Hebb’s postulate
when an axon of cell A excites a cell B axon and repeatedly takes part in firing, some growth processes or metabolic changes take place in one or both cells so that A’s efficiency as one of the cells firing B is increased.
properties of LTP
-input specific (LTP only at synapses)
-cooperativity (many axons needed to pass threshold)
-associativity (little stimulation at same time can cause LTP)
what does an increase in synaptic transmission cause
increased conductivity of AMPAR
increased density of AMPAR
more synaptic vesicle release
what does LTP induction require
NMDAR (coincidence detector)
postsynaptic depolarisation
steps in LTP induction
glutamate opens NMDA channel
Ca-CaM activates kinases
phosphorylates AMPAr
more Na+ entry
more receptors
what type of signalling occurs in LTP induction
retrograde signalling
gases (NO)
act pre synaptically so more NT release
what occurs after LTP induction
immediate structural changes,
input specific change
role of CaMKII
trafficking and phosphorylation of AMPAR
where does CaMKII autophosphorylation occur
Thr 286
inhibits CaM activity
role of CaMKII activity reporter
2 flurophores: dimVenus/mEGF
colour code fluorscence
high activity = warm colours
what does CaMKII activity occulude
LTP induction
what is CamKII autophosphorylation required for
CA1-LTP
not for DG-LTP
what are silent synapses
functional NMDA receptors
no AMPA receptors
what occurs in the developing hippocampus
silent synapses and LTP induction
how to obtain late-LTP
gene transcription and protein synthesis induction and multiple tetani in brain slices
what gene is transcribed after synaptic stimulation
c-fos (immediately early gene)
role of synaptic tagging/synaptic culture
enables input specificity and a type of associativity
tag setting -> PRP capture ->L-LTP
how is experimental evidence collected for synaptic tagging
using a protein synthesis blocker
role of PKMzeta in LTP maintenance
prevents endocytosis of AMPAR
and phosphorylates synapses
PIN1 - inhibitor of own mRNA translation
role of ZIP (zeta inhibitory peptide)
erases LTP after consolidation but is not specific
different types of LTP
brain region (CA1/DG)
age (juvenile/adult/aged)
stimulation frequency (E-LTP/L-LTP)
what does LTD stand for
long term depression
what does LTD stimulation cause
dephosphorylation and endocytosis
low frequency NMDAR activation
age dependence of LTD induction
NMDAR subunits change with age. NR2B containing NMDARs are more permeable to calcium and is more abundant in post natal development.
2 types of LTD in CA1
NMDAR-LTD (low ca2+, phosphatases)
mGluR-LTD (activates PKC, phosphorylates AMPAR)
what is spike timing dependent plasticity (STDP)
timing of presynaptic & postsynaptic firing determines whether LTD/LTP induced, or whether synaptic transmission does not change
LTD in cerebellum
parallel fibres from granule cell
mossy fibre
climbing fibre
purkinje cell
output is inhibitory neurons
LTD at parallel fibre-purkinje cell synapses
long lasting
input specific
cooperativity (threshold stimulation needed)
coinciding input at parallel fibre & climbing fibre synapses
role of pf-PC LTD
important for cerebellar learning
