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Regulation of Presynaptic Ca(V)2.1 Channels by Ca2+ Sensor Proteins Mediates Short-Term Synaptic Plasticity

Regulation of Presynaptic Ca(V)2.1 Channels by Ca2+ Sensor Proteins Mediates Short-Term Synaptic Plasticity

Sumiko Mochida, Alexandra P Few, Todd Scheuer, William A Catterall

Neuron. 2008 Jan 24;57(2):210-6.

PMID: 18215619

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+) current markedly reduces facilitation of synaptic transmission. Deletion of the nearby calmodulin-binding domain, which inhibits CaS-dependent inactivation, substantially reduces depression of synaptic transmission. These results demonstrate that residual Ca(2+) in presynaptic terminals can act through CaS-dependent regulation of Ca(V)2.1 channels to induce short-term synaptic facilitation and rapid synaptic depression. Activity-dependent regulation of presynaptic Ca(V)2.1 channels by CaS proteins may therefore be a primary determinant of short-term synaptic plasticity and information-processing in the nervous system.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP115044694-A	Calmodulin Binding Domain - CAS 115044-69-4		115044-69-4	Price

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