Neuron
ArticleRole of residual calcium in synaptic depression and posttetanic potentiation: Fast and slow calcium signaling in nerve terminals
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Dynamic compartmentalization of calcium channel signalling in neurons
2020, NeuropharmacologyCitation Excerpt :The spatial proximity of VGCCs to the calcium sensor of SVs is the key parameter of efficient coupling between VGCC opening and SV release that was discussed in detail in excellent recent reviews (Bohme et al., 2018; Eggermann et al., 2012; Stanley, 2016; Sudhof, 2013). Due to the defined readout of synaptic activity and the knowledge of conductance properties of VGCCs, the size and extension of calcium nanodomains can be well defined by exogenous calcium buffers (Adler et al., 1991; Schneggenburger and Neher, 2000; Swandulla et al., 1991) and have been used to explore nanodomain signalling along the neuronal membrane. Other examples for tight coupling between VGCC and calcium-gated or -modulated ion channels or calcium-sensitive enzymes revealed that tight coupling between VGCCs and effector molecules reflects a common feature of fast calcium signalling (Berkefeld et al., 2006; Constantin et al., 2017).
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2008, NeuronCitation Excerpt :For example, at the squid giant synapse, both facilitation and depression clearly occur in the absence of any changes in presynaptic calcium currents (Charlton et al., 1982). At this synapse, augmentation also occurs in the absence of any obvious changes in presynaptic calcium influx (Swandulla et al., 1991). Even for the case of the synapses examined by Mochida et al. (2008), some facilitation persists after both of the CaS-protein-binding sites of the calcium channel were mutated (Figure 2B of Mochida et al., 2008), and some depression is evident during repeated synaptic activity even after the calmodulin binding domain is deleted (Figure 3B).
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Present address: Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139.