…Neuronal Complexity…
Synaptic Modulation
Things get more complicated in a real
world of neural connections:
Inputs from excitatory and inhibitory synapses
are received in the integrating segment of the
post-synaptic neurone and a response is
produced in the spike initiation zone. This is
summation (several received signals).
Complex forms of synaptic
activity…
A single neurone can have many thousands of inputs and synapse
onto a vast number of other cells/neurones.
This results in very complex circuits being formed.
Although the nervous system can be compared to a computer in
many ways when we consider the biology of these large networks
many of the “computer like” properties are lost
This is because the nervous system has properties that are very
biological.
Facilitation…
two or more action potentials reach the presynaptic terminals in a
short period of time
more neurotransmitter released per action potential
stronger response in the post synaptic neurone – increased
effectiveness of the connection to the post-synaptic neurone
frequently used pathways become more
effective pathways.
Forms of short-term synaptic plasticity:
synaptic facilitation:
Change in post-synaptic membrane
potential measured as greater after
facilitation. More NT released, binds to
more receptors, more opening of
channels and greater change in
membrane potential. Has knock-on
effects for the activity of the post-
synaptic neurone – makes it more likely that the post-synaptic cell
, will generate an action potential. Increased rate of neural activity in
the pathway.
Dependence of facilitation on spike interval:
Spike interval = the rate at which action potentials
invade the pre-synaptic terminus and induce release
of neurotransmitter. As the interval between stimuli
decreases, the amount of facilitation in the post-
synaptic neurone is higher.
Depression…
A rapid succession of action potentials is termed a tetanic train. The
first response of a synapse to a tetanic train is depression.
Tetanic trains can cause depletion neurotransmitter
- Result in decreased neurotransmitter release into synapse
- Decreased EPSPs (excitatory post-synaptic potentials) -
depression. Decrease in post-synaptic response.
Recovery depression causes
change in calcium
dependent processes -
synaptic vesicles available
per incoming action
potential, to a short - term
enhancement of the
synapse’s activity termed:
- Post-tetanic
potentiation (third kind of short term synaptic plasticity)
Probability of transmitter release and short-term plasticity:
Depression and facilitation are
the two main kinds of short-term
plasticity. Cause a decrease/
increase in the amplitude of the
post-synaptic potential.
Note: these changes are pre-
synaptic while summation is
post-synaptic. Here, change
post-synaptic membrane potential resulting in ion channels opening
is measured rather than action potential itself. However, the change
is measured post-synaptically in both cases.
Pre-synaptic parameters influencing short-term plasticity
Local intracellular calcium
concentration: neurotransmitter release
depends on availability of calcium ions
to bind to vesicle membranes and
trigger fusion and release of synaptic
vesicles into the cleft.
Synaptic Modulation
Things get more complicated in a real
world of neural connections:
Inputs from excitatory and inhibitory synapses
are received in the integrating segment of the
post-synaptic neurone and a response is
produced in the spike initiation zone. This is
summation (several received signals).
Complex forms of synaptic
activity…
A single neurone can have many thousands of inputs and synapse
onto a vast number of other cells/neurones.
This results in very complex circuits being formed.
Although the nervous system can be compared to a computer in
many ways when we consider the biology of these large networks
many of the “computer like” properties are lost
This is because the nervous system has properties that are very
biological.
Facilitation…
two or more action potentials reach the presynaptic terminals in a
short period of time
more neurotransmitter released per action potential
stronger response in the post synaptic neurone – increased
effectiveness of the connection to the post-synaptic neurone
frequently used pathways become more
effective pathways.
Forms of short-term synaptic plasticity:
synaptic facilitation:
Change in post-synaptic membrane
potential measured as greater after
facilitation. More NT released, binds to
more receptors, more opening of
channels and greater change in
membrane potential. Has knock-on
effects for the activity of the post-
synaptic neurone – makes it more likely that the post-synaptic cell
, will generate an action potential. Increased rate of neural activity in
the pathway.
Dependence of facilitation on spike interval:
Spike interval = the rate at which action potentials
invade the pre-synaptic terminus and induce release
of neurotransmitter. As the interval between stimuli
decreases, the amount of facilitation in the post-
synaptic neurone is higher.
Depression…
A rapid succession of action potentials is termed a tetanic train. The
first response of a synapse to a tetanic train is depression.
Tetanic trains can cause depletion neurotransmitter
- Result in decreased neurotransmitter release into synapse
- Decreased EPSPs (excitatory post-synaptic potentials) -
depression. Decrease in post-synaptic response.
Recovery depression causes
change in calcium
dependent processes -
synaptic vesicles available
per incoming action
potential, to a short - term
enhancement of the
synapse’s activity termed:
- Post-tetanic
potentiation (third kind of short term synaptic plasticity)
Probability of transmitter release and short-term plasticity:
Depression and facilitation are
the two main kinds of short-term
plasticity. Cause a decrease/
increase in the amplitude of the
post-synaptic potential.
Note: these changes are pre-
synaptic while summation is
post-synaptic. Here, change
post-synaptic membrane potential resulting in ion channels opening
is measured rather than action potential itself. However, the change
is measured post-synaptically in both cases.
Pre-synaptic parameters influencing short-term plasticity
Local intracellular calcium
concentration: neurotransmitter release
depends on availability of calcium ions
to bind to vesicle membranes and
trigger fusion and release of synaptic
vesicles into the cleft.
