α1E-containing Ca2+ channels are involved in synaptic plasticity

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Item Type:	Article
Title:	α1E-containing Ca2+ channels are involved in synaptic plasticity
Creators Name:	Breustedt, J., Vogt, K.E., Miller, R.J., Nicoll, R.A. and Schmitz, D.
Abstract:	Long-term potentiation (LTP) is the most prominent model for the molecular and cellular mechanisms of learning and memory. Two main forms of LTP have been distinguished. The N-methyl-D-aspartate-receptor-dependent forms of LTP have been studied most extensively, whereas much less is known about N-methyl-D-aspartate-receptor-independent forms of LTP. This latter type of LTP was first described at the mossy fiber synapses in the hippocampus and subsequently at parallel fiber synapses in the cerebellum as well as at corticothalamic synapses. These presynaptic forms of LTP require a rise in the intraterminal calcium concentration, but the channel through which calcium passes has not been identified. By using pharmacological tools as well as genetic deletion, we demonstrate here that {alpha}1E-containing voltage-dependent calcium channels (VDCCs) shift the threshold for mossy fiber LTP. The channel is not involved in the expression mechanism, but it contributes to the calcium influx during the induction phase. Indeed, optical recordings directly show the presence and the function of {alpha}1E-containing VDCCs at mossy fiber terminals. Hence, a previously undescribed role for {alpha}1E-containing VDCCs is suggested by these results.
Keywords:	Calcium Channel Blockers, Calcium Channels, Calcium Signaling, Cation Transport Proteins, Hippocampal Mossy Fibers, Long-Term Potentiation, Neuronal Plasticity, {omega}-Agatoxin IVA, R-Type Calcium Channels, Spider Venoms, Synaptic Transmission, Animals, Rats
Source:	Proceedings of the National Academy of Sciences of the United States of America
ISSN:	0027-8424
Publisher:	National Academy of Sciences
Volume:	100
Number:	21
Page Range:	12450-12455
Date:	14 October 2003
Official Publication:	https://doi.org/10.1073/pnas.2035117100
PubMed:	View item in PubMed

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