2008
DOI: 10.1016/j.neuron.2007.11.036
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Regulation of Presynaptic CaV2.1 Channels by Ca2+ Sensor Proteins Mediates Short-Term Synaptic Plasticity

Abstract: Short-term synaptic plasticity shapes the postsynaptic response to bursts of impulses and is crucial for encoding information in neurons, but the molecular mechanisms are unknown. Here we show that activity-dependent modulation of presynaptic Ca(V)2.1 channels mediated by neuronal Ca(2+) sensor proteins (CaS) induces synaptic plasticity in cultured superior cervical ganglion (SCG) neurons. A mutation of the IQ-like motif in the C terminus that blocks Ca(2+)/CaS-dependent facilitation of the P/Q-type Ca(2+) cur… Show more

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Cited by 143 publications
(203 citation statements)
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“…Interestingly, it has been recently reported that the activity-dependent regulation of presynaptic CaV2.1 channels by Ca ?? sensor proteins (CaS proteins) may be a primary determinant of short-term synaptic plasticity and information-processing in the nervous system (Mochida et al 2008). Such processes would also occur near plasma membrane.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, it has been recently reported that the activity-dependent regulation of presynaptic CaV2.1 channels by Ca ?? sensor proteins (CaS proteins) may be a primary determinant of short-term synaptic plasticity and information-processing in the nervous system (Mochida et al 2008). Such processes would also occur near plasma membrane.…”
Section: Discussionmentioning
confidence: 99%
“…Activity-dependent increases in presynaptic calcium influx (independent of waveform changes) following tetanic stimulation could contribute to PTP Inchauspe et al 2004;Ishikawa et al 2005;Habets and Borst 2006). However, studies of cultured superior cervical ganglion synapses suggest that facilitation of calcium entry could contribute to synaptic augmentation but not PTP (Mochida et al 2008). …”
Section: Short-term Presynaptic Plasticitymentioning
confidence: 99%
“…At the calyx of Held synapse, short-term depression is largely a result of decreased calcium entry for activation frequencies of ,30 Hz and primarily a result of depletion at frequencies .100 Hz; at intermediate frequencies both mechanisms contribute (Xu and Wu 2005). Studies of synaptic transmission in cultured superior cervical ganglion neurons expressing calcium channels that either possess or lack calmodulin-dependent inactivation suggest that depression can arise from calcium channel inactivation mediated by calmodulin (Mochida et al 2008). …”
Section: Inactivation Of Calcium Channels and Other Mechanisms Of Depmentioning
confidence: 99%
See 1 more Smart Citation
“…Ca V 2.1 channels are regulated by binding of calmodulin (CaM) and related calcium sensor proteins to a bipartite binding site in the C-terminal domain, leading to Ca 2+ -dependent facilitation (CDF) and Ca 2+ -dependent inactivation (CDI) during trains of depolarizing stimuli (10)(11)(12)(13). Recent work has shown that these forms of Ca 2+ -dependent regulation of presynaptic Ca 2+ channels modulate synaptic transmission to produce short-term facilitation and short-term depression (14)(15)(16)(17). To explore the possible role of presynaptic Ca 2+ channels as a source of Ca 2+ entry that triggers asynchronous neurotransmitter release, we searched for a form of Ca 2+ -dependent regulation of Ca V 2 channels that could contribute to asynchronous neurotransmitter release.…”
mentioning
confidence: 99%