Short-term synaptic plasticity

Figure 1. Presynaptic mechanisms of use-dependent short-term plasticity. Schematic diagrams illustrate proposed mechanisms for depression (a), facilitation (b), and post-tetanic potentiation (PTP) and augmentation (c). RRP: readily releasable pool of vesicles; Cares: residual calcium.

Site and mechanism of Ca2+ channel regulation. A, presynaptic Ca2+channel signaling complex. Sites of interaction of SNARE proteins (the synprint site) and CaM and CaS proteins on the α1 subunit are illustrated. B, model for sequential Ca2+/CaM-dependent facilitation and inactivation. Local rises in intracellular Ca2+ activate the two C-terminal Ca2+-binding EF-hands of CaM, strengthening interaction with the IQ-like motif and causing facilitation. Following prolonged Ca2+ entry, global rises in intracellular Ca2+ allow CaM to become fully liganded and to interact with both the IQ-like motif and CBD to produce inactivation. This figure was reproduced from Ref. 12 with permission.

mechanisms

Calcium channel regulation