Ca²⁺/Calmodulin and Presynaptic Short-Term Plasticity

Figure 1

Presynaptic facilitation and depression mediated by Ca_V2.1 channel facilitation and inactivation. (a) Averaged trace of EPSPs (𝑛=5−12), in which Ca_V2.1 channels were the only active channels in the presence of ω-conotoxin GVIA, evoked by action potentials with 1 s train at 30 Hz. (b) Normalized amplitudes of EPSPs recorded every 2 s in the presence of ω-Conotoxin GVIA. Conditioning stimuli were applied at the indicated times at 20 Hz for 10 s to evoke augmentation and at 20 Hz for 60 s to induce PTP. Adapted from Mochida et al., 2008 [26]. (c) Model illustrating Ca_V2.1-mediated mechanisms of synaptic depression, facilitation, and augmentation. In synaptic depression, CaM sensing local Ca²⁺ interacts with the CaM-binding domain (CBD) to cause channel inactivation and reduce Ca²⁺ entry, thus, reducing neurotransmitter release. In synaptic facilitation and augmentation, CaM sensing global Ca²⁺ interacts with the IQ-like motif to cause channel facilitation and increase in Ca²⁺ entry, and subsequently neurotransmitter release increases.