CJH332H1 Lecture Notes - Lecture 12: Synaptic Plasticity, Chemical Synapse, Long-Term Memory
Lecture 12: Altering Synapses I Physiology
Key feature of synaptic plasticity
• Change in the strength of synapse persists after the activity (train of APs) that induced the plasticity has ceased
Synaptic plasticity – what it looks like
• Changes in presynaptic electrical activity (APs) can alter the synaptic efficacy (brief strengthening of synapse)
• A brief train of APs (presynaptic activity) can cause either an increase (facilitation) or a decrease (depression) in
the size of the postsynaptic potentials (EPSPs or IPSPs)
Augmentation in synaptic plasticity
• Slower phase than that of facilitation
• Repetitive stimulation also induces augmentation – an increase in
synaptic potential amplitude
• Augmentation comes on more slowly than facilitation and decays more
slowly (5-10 sec)
• Also due to an increase in the amount of transmitter being released pre synaptically
Synaptic depression
• Reduction of transmitter release from presynaptic terminals due to previous synaptic activity – thought to be
due to a depletion of vesicles for neurotransmission (after Ca2+ influx)
• One place this is sometimes observed by tetanus stimulation of high-frequency train of APs (prolonged)
- Presynaptic and postsynaptic neurotrasitters are ot released as effectively (do’t get the sae stregth
of response – another form of plasticity)
- Weakening of synapse for control of activity in brain, block unnecessary information AND resetting synapses
for good memory and learning
• Depression often followed after a few seconds by an increase in synaptic potential amplitude – post-tetanic
potentiation (PTP)
Facilitation and depression
• Facilitation is due to an increase in the mean number of quanta released by the presynaptic nerve terminal
- Number of quanta released more than doubles
- Due to residual Ca2+ left in the presynaptic terminal
• Depression is mostly due to depletion of vesicles from the nerve terminal during the conditioning trains of APs
- Cannot fill the vesicles fast enough with neurotransmitters
• Neurotransmitter release is subject to 2 short-term modifications
- Facilitation – over the immediate short-term, due to an increase in efficacy of release of quanta
- Depression – occurring slightly later, depletion of vesicles/quanta that produces a reduced efficacy of
neurotransmitter release
Post-tetanic Potentiation (PTP)
• PTP in synaptic plasticity (short term) is an increase in the synaptic potential amplitude due to increase
neurotransmitter released (exact mechanism still remains unknown)
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Key feature of synaptic plasticity: change in the strength of synapse persists after the activity (train of aps) that induced the plasticity has ceased. Presynaptic and postsynaptic neurotra(cid:374)s(cid:373)itters are (cid:374)ot released as effectively (do(cid:374)"t get the sa(cid:373)e stre(cid:374)gth of response another form of plasticity) Facilitation and depression: facilitation is due to an increase in the mean number of quanta released by the presynaptic nerve terminal. Number of quanta released more than doubles. Due to residual ca2+ left in the presynaptic terminal: depression is mostly due to depletion of vesicles from the nerve terminal during the conditioning trains of aps. Cannot fill the vesicles fast enough with neurotransmitters: neurotransmitter release is subject to 2 short-term modifications. Facilitation over the immediate short-term, due to an increase in efficacy of release of quanta. Depression occurring slightly later, depletion of vesicles/quanta that produces a reduced efficacy of neurotransmitter release. Long-term changes in synaptic signaling: cns synaptic plasticity is often long-term.
