CJH332H1 Lecture Notes - Lecture 11: Dentate Gyrus, Long-Term Potentiation, Long-Term Depression
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
• One place this is sometimes observed by tetanus stimulation high frequency train of APs (prolonged)
• Depression often followed after a few seconds by an increase in synaptic
potential amplitude – Post-Tetanic Potentiation (PTP)
Facilitation and depression
• The initial effect of facilitation outweighs that of depression; thus the
responses increase in amplitude
• When the test pulse is given (on the right side of diagram), facilitation has
partially worn off and is overridden by depression, which has a more prolonged time course and tends to last
longer
• Facilitation is due to an increase in the mean number of quanta released by the presynaptic nerve terminal; the
number of quanta released more than doubles
- Possibly due to residual Ca2+ left in the presynaptic terminal
• Depression mostly due to the depletion of vesicles from the nerve terminal during the conditioning train of APs
• Thus, transmitter release is subject to 2 short-term modifications: facilitation (over the immediate short-term:
due to and increase in efficacy of release of quanta) and then depression (occurring slightly later: depletion of
vesicles/quanta that produces a reduced efficacy of neurotransmitter release)
Post-tetanic Potentiation (PTP)
• PTP in synaptic plasticity is an increase in the synaptic potential amplitude due to increase transmitter release
- The exact mechanism still remains unknown
• Delayed onset: maximum amplitude for PTP is reached seconds after stimulation ends and lasts tens of minutes
Example of PTP
• Potentials were recorded with an intracellular microelectrode
• Treated with curare to decrease the EPSP amplitude
• Cell was hyper-polarized prior to stimulation to prevent an AP
• An initial electrical coupling potential
• The second slower depolarization is caused by ACh release and binding
• Stimulus = 100pulses/s for 15 seconds (1500 stimuli)
Long term changes in synaptic signaling
• CNS synaptic plasticity is often long term (short term changes are seen more commonly at peripheral synapses)
• 2 types of long term changes
- LTP – long term potentiation
- LTD – long term depression
- LTP and LTD are though to be cellular basis of learning and memory among other behavioral effects
LTP and LTD
• LTP – increase in size of a synaptic potential lasting hours or more, produced by previous synaptic activity
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Document Summary
Post-tetanic potentiation (ptp: ptp in synaptic plasticity is an increase in the synaptic potential amplitude due to increase transmitter release. The exact mechanism still remains unknown: delayed onset: maximum amplitude for ptp is reached seconds after stimulation ends and lasts tens of minutes. Long term changes in synaptic signaling: cns synaptic plasticity is often long term (short term changes are seen more commonly at peripheral synapses, 2 types of long term changes. Ltp and ltd are though to be cellular basis of learning and memory among other behavioral effects. Ltp increase in size of a synaptic potential lasting hours or more, produced by previous synaptic activity. Ltd decrease in size of a synaptic potential lasting hours or more, produced by previous synaptic activity. Ltp in hippocampus of anesthetized rabbit: tetanic stimuli (15/s for 10 sec) to pp record from granule cells in the dg, stimuli given at arrows, red dots are stimulated pathways and blue for control.
