Synaptic plasticity chapter 8
Learning objectives: Synaptic depression
• Be able to discuss the different forms of short-term synaptic The opposite of synaptic facilitation is synaptic depression, which
plasticity causes a decline in neurotransmitter release during synaptic
• Explain how calcium shapes synaptic plasticity by affecting activity. Depression depends on the amount of neurotransmitter
neurotransmitter release that has been released. The total amount of depression is
• Describe Aplysia’s behavioural responses during habituation and proportional to the amount of transmitter that is released from
sensitisation the presynaptic terminal. This means that depression is caused by
• Explain the neuronal circuitry that facilitates gill withdrawal the depletion of a pool of synaptic vesicles that are available for
and sensitisation release. When rates of release are high, the vesicles deplete
• Know the molecular pathways that govern short- and long- rapidly and cause a lot of depression.
term sensitisation
• Have a basic understanding of the hippocampal neurocircuitry Synaptic potentiation and augmentation
from the entorhinal cortex to CA1 pyramidals These types of plasticity serve to increase the amount of
• Be able to describe the three principles of long-term synaptic transmitter released from presynaptic terminals. Both
plasticity. Namely, specificity, state dependence and associativity augmentation and potentiation enhance the ability of incoming
• Understand the contribution of AMPA and NMDA receptors and calcium to trigger the fusion of synaptic vesicles with the plasma
the downstream signalling in LTP membrane, but the two processes work over different timescales.
• Recognise and understand the differences in the downstream Augmentation works throughout a few seconds and potentiation
mechanisms between LTP and LTD acts over a timescale of seconds to minutes.
Chemical synapses are capable of undergoing plastic changes Overview
that either strengthen or weaken synaptic transmission. Synaptic
plasticity mechanisms occur on timescales ranging from
milliseconds to days, weeks, or even longer. There are two forms
of synaptic plasticity:
• Short-term plasticity (presynaptic side)
• Long-term plasticity
Short-term synaptic plasticity
Several forms of short-term synaptic plasticity differ in time In this graph, you can see that when there is stimulation there is
courses and underlying mechanisms. facilitation, augmentation and eventually potentiation. Due to the
potentiation and the constant stimuli, the vesicle pools are
Synaptic facilitation depleted and there is depression. When the constant stimulation
Synaptic facilitation is a rapid increase in synaptic strength that stops for a few milliseconds the vesicles have time to be refilled.
occurs when two repeated action potentials invade the After a few minutes, there is a membrane potential that is still
presynaptic terminal within a few milliseconds of each other, a quite high due to the calcium residues that were present. They
paired pulse facilitation. This causes a calcium influx and the
·
call this post-tetanic potentiation (PTP).
release of a synaptic vesicle. The repeated action potentials
cause a calcium build-up which allows more synaptic vesicles to Long-term synaptic plasticity
be released. If you would chance the interval of the stimuli you This type of plasticity lasts for longer than 30 minutes and is
see that when the time between two pulses is increased, there responsible for changes in brain function that persist for weeks,
is less facilitation and there are less vesicles being released. months, or years. Because of their duration, these forms of
After 15ms there is no facilitation anymore. The target of this synaptic plasticity may be correlated with learning and memory.
calcium signal is synaptotagmin, which is a calcium-binding protein
that is found on the plasma membrane (also on synaptic vesicles Behavioural modification in Aplysia
where they function as calcium sensors and trigger The Aplysia is a sea slug that has a very simple nervous system.
neurotransmitter release). Aplysia exhibits several forms of behavioural plasticity.
• Habituation: causes the animal to become less responsive to
repeated stimuli (a form of depression)
• Sensitisation: this allows the animal to enhance a response
upon aversive stimulus (a form of facilitation)
Residual calcium
Learning objectives: Synaptic depression
• Be able to discuss the different forms of short-term synaptic The opposite of synaptic facilitation is synaptic depression, which
plasticity causes a decline in neurotransmitter release during synaptic
• Explain how calcium shapes synaptic plasticity by affecting activity. Depression depends on the amount of neurotransmitter
neurotransmitter release that has been released. The total amount of depression is
• Describe Aplysia’s behavioural responses during habituation and proportional to the amount of transmitter that is released from
sensitisation the presynaptic terminal. This means that depression is caused by
• Explain the neuronal circuitry that facilitates gill withdrawal the depletion of a pool of synaptic vesicles that are available for
and sensitisation release. When rates of release are high, the vesicles deplete
• Know the molecular pathways that govern short- and long- rapidly and cause a lot of depression.
term sensitisation
• Have a basic understanding of the hippocampal neurocircuitry Synaptic potentiation and augmentation
from the entorhinal cortex to CA1 pyramidals These types of plasticity serve to increase the amount of
• Be able to describe the three principles of long-term synaptic transmitter released from presynaptic terminals. Both
plasticity. Namely, specificity, state dependence and associativity augmentation and potentiation enhance the ability of incoming
• Understand the contribution of AMPA and NMDA receptors and calcium to trigger the fusion of synaptic vesicles with the plasma
the downstream signalling in LTP membrane, but the two processes work over different timescales.
• Recognise and understand the differences in the downstream Augmentation works throughout a few seconds and potentiation
mechanisms between LTP and LTD acts over a timescale of seconds to minutes.
Chemical synapses are capable of undergoing plastic changes Overview
that either strengthen or weaken synaptic transmission. Synaptic
plasticity mechanisms occur on timescales ranging from
milliseconds to days, weeks, or even longer. There are two forms
of synaptic plasticity:
• Short-term plasticity (presynaptic side)
• Long-term plasticity
Short-term synaptic plasticity
Several forms of short-term synaptic plasticity differ in time In this graph, you can see that when there is stimulation there is
courses and underlying mechanisms. facilitation, augmentation and eventually potentiation. Due to the
potentiation and the constant stimuli, the vesicle pools are
Synaptic facilitation depleted and there is depression. When the constant stimulation
Synaptic facilitation is a rapid increase in synaptic strength that stops for a few milliseconds the vesicles have time to be refilled.
occurs when two repeated action potentials invade the After a few minutes, there is a membrane potential that is still
presynaptic terminal within a few milliseconds of each other, a quite high due to the calcium residues that were present. They
paired pulse facilitation. This causes a calcium influx and the
·
call this post-tetanic potentiation (PTP).
release of a synaptic vesicle. The repeated action potentials
cause a calcium build-up which allows more synaptic vesicles to Long-term synaptic plasticity
be released. If you would chance the interval of the stimuli you This type of plasticity lasts for longer than 30 minutes and is
see that when the time between two pulses is increased, there responsible for changes in brain function that persist for weeks,
is less facilitation and there are less vesicles being released. months, or years. Because of their duration, these forms of
After 15ms there is no facilitation anymore. The target of this synaptic plasticity may be correlated with learning and memory.
calcium signal is synaptotagmin, which is a calcium-binding protein
that is found on the plasma membrane (also on synaptic vesicles Behavioural modification in Aplysia
where they function as calcium sensors and trigger The Aplysia is a sea slug that has a very simple nervous system.
neurotransmitter release). Aplysia exhibits several forms of behavioural plasticity.
• Habituation: causes the animal to become less responsive to
repeated stimuli (a form of depression)
• Sensitisation: this allows the animal to enhance a response
upon aversive stimulus (a form of facilitation)
Residual calcium
