Multiple overlapping processes underlying short-term synaptic enhancement.
By Stephen A. Fisher, T. M. Fischer, T. J. Carew. 1997
Recently there have been exciting advances in understanding the mechanisms and functional roles of a form of short-term synaptic enhancement (STE) that results from an activity-dependent accumulation of Ca2+ in the presynaptic terminal. This form of STE is composed of at least four processes: fast-decaying facilitation (FI), slow-decaying facilitation (F2), augmentation (AUG) and post-tetanic potentiation (PTP). Recent results suggest that these processes can now be distinguished mechanistically by the site of their induction within the presynaptic terminal: FI and F2 appear to be induced by a rapid, high concentration of Ca2+ at or near the site of exocytosis, whereas AUG and PTP seem to be induced by lower levels of Ca2+ with slower kinetics, possibly within the core of the terminal. STE is highly conserved across diverse species, and appears to serve as a flexible mechanism for temporal information processing in systems ranging from peripheral motor control to higher cortical integration.
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Citations in the corpus
- Decoding Temporal Information: A Model Based on Short-Term Synaptic Plasticity (2000, background): “, 1997), it has also been suggested that short-term plasticity may provide a mechanism for “on-line” modulation in certain types of behaviors (Fisher et al., 1997).”
- Short-term synaptic plasticity. (2002, background): “residual [Ca2+]i, (5) reserve pool, (6) metabotropic autoreceptors, (7) ionotropic autoreceptors, (8) Ca 2+-ATPase, regulating residual [Ca 2+]i in augmentation, (9) mitochondrial regulation of residual [Ca 2+]i in PTP, (10) postsynaptic receptor desensitization.”