Biology Reference
In-Depth Information
processing and self-regulation of neural networks. Synaptic efficacy is dynamic. For
instance, when closely spaced action potentials reach a presynaptic terminal, the synapse does
not transmit them identically to a postsynaptic neuron. This form of synaptic plasticity,
termed short-term plasticity, is diverse. At facilitating synapses, the postsynaptic responses to
later spikes in repetitive presynaptic firing are larger than that to the first one, whereas at
depressing synapses, they are smaller. Whether a synapse is facilitating or depressing depends
upon the type of synapse. Hippocampal mossy fibre- CA3 synapses and climbing fiber-
Purkinje cell synapses are typically facilitating, whereas parallel fiber- Purkinje cell synapses
display depression. However, the biophysical mechanisms underlying short-term plasticity
are multiple and complex, and therefore in many types of synapses, including hippocampal
Schaffer collateral-CA1 synapses, these two forms of plasticity, i.e., facilitation and
depression, often coexist, resulting in complicated profiles of short-term plasticity.
Table 1. Activity dependent synaptic mechanisms, a rough estimate of their decay
constants and an indication of whether they are depending on pre
-
or postsynaptic
activity or both are given [123, 212]
Mechanism
Duration
Synaptic Location
Short-term Plasticity
Paired-pulse facilitation (PPF)
Augmentation
Post-tetanic potentiation (PTP)
Depolarization-induced suppression of
inhibition (DSI)
Depolarization-induced suppression of
excitation (DSE)
Paired pulse depression (PPD)
Depletion
100 ms
10 s
1 min
50 -75 ms
50 -75 ms
100 ms
10s
15 min
> 30 min
>30 min
Pre
Pre
Pre
Pre
Pre
Pre
Pre
Post
Pre and Post
Pre and Post
Long-term plasticity
Short-term Potentiation (STP)
Long-term Potentiation (LTP)
Long-term depression (LTD)
Short-term synaptic enhancement has been most thoroughly characterized at invertebrate
synapses and at the neuromuscular junction in vertebrates [8, 129]. High-frequency stimulus
trains enhance release both during and after stimulation. Based upon differences in time
course and pharmacology, this enhancement is separated into four components: post tetanic
potentiation (PTP), augmentation, facilitation component F2, and facilitation component Fl,
with time constants of decay of 30-90 set, 5-10 set, 200-500 msec, and 20-l00 msec,
respectively. Quanta1 analysis indicates that these forms of enhancement are presynaptic in
origin. Short-term memory involves modifications of preexisting proteins and transient
strengthening of preexisting synaptic connections.
