Mechanisms at the terminal level for synaptic enhancement on several time-scales (facilitation, augmentation, post-tetanic potentiation) and depression will be discussed. Issues to be considered will include the roles of residual free Ca2+ and residual Ca2+ bound to ``memory proteins", and the roles of domain and macroscopic Ca2+. We will also explore to what extent synaptic depression can be accounted for in terms of vesicle depletion and resupply.

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