Multiple roles of calcium ions in the regulation of neurotransmitter release.

By E. Neher, T. Sakaba. Neuron, 2008

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Burst timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons: A putative cellular substrate for reward learning (2009, neutral): “, 2008; Zucker and Regehr, 2002) involving classical vesicle depletion and presynaptic Ca accumulation (Neher and Sakaba, 2008) as well as enhancement of release machinery via phosphorylation (Evans and Morgan, 2003; Leenders and Sheng, 2005), cannabinoid-”
Short-term presynaptic plasticity. (2012, background): “According to a second model of synaptic depression, fusion of a vesicle at an active zone can inhibit subsequent fusion of available vesicles for several seconds (Betz 1970; Kusano and Landau 1975; Varela et al. 1997; Dittman and Regehr 1998; Neher and Sakaba 2008).”
SNARE Protein Recycling by aSNAP and bSNAP Supports Synaptic Vesicle Priming (2010, positive): “To discern whether the impairment of the slow flash-induced release phase in DMut neurons is due to a defect in basal RRP refilling rates or to a deficiency in the activity-dependent augmentation of SV priming (Neher and Sakaba, 2008), we measured priming rates at basal and high [Ca2+]i.”