In:
eLife, eLife Sciences Publications, Ltd, Vol. 6 ( 2017-08-08)
Abstract:
The points of contact between nerve cells are called synapses, and nerve cells communicate across synapses via chemicals known as neurotransmitters. These chemical messengers are initially stored within bubble-like packages called synaptic vesicles that are released after they fuse with the membrane of the nerve cell at a specialized site referred to as the “active zone”. Calcium ions are one of the major factors that lead to the release of synaptic vesicles. Ion channel proteins in the membrane of the nerve cell control the flow of calcium ions into the cell. There are often many different ion channels at a synapse, but one type called CaV2.1 most effectively triggers the release of synaptic vesicles when a nerve impulse reaches the synapse. Various proteins at the active zone can bind directly to parts of the CaV2.1 channel that are identified by a short sequence of amino acids – the building blocks of all proteins. Several researchers have proposed that the interactions with some of these short sequences, which are also known as motifs, control how much of this ion channel is in the synapse and how it interacts with synaptic vesicles to regulate the release of neurotransmitters. However, other researchers do not agree with this proposed explanation. Lübbert, Goral et al. set out to determine which parts in a specific part of the CaV2.1 channel (called the “α1 subunit C-terminus”) are critical for its interaction with synaptic vesicles. The experiments revealed a new motif that regulates how many synaptic vesicles could be released in response to electrical impulses travelling along nerve cells from mice. The same motif also regulates the total number of synaptic vesicles at the active zone. Lübbert, Goral et al. went on to show that binding to known active proteins at most played a minor role in controlling the abundance of the CaV2.1 channels and how close they were to the synaptic vesicles. As such, these findings counter prevailing views of the roles of certain motifs in the α1 subunit of the CaV2.1 channel. Thus, it may be necessary to re-think how the CaV2.1 channel regulates the release of synaptic vesicles. Ion channels are vital to the activity of all nerve cells, and working out how the numbers and organization of CaV2.1 and related ion channels are regulated will be fundamental to understanding how information is encoded in brain. In addition, problems with these kinds of ion channel may result in disorders such as migraines and epilepsy. Therefore, the new findings may help to guide further studies investigating possible ways to treat these disorders.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.28412.001
DOI:
10.7554/eLife.28412.002
DOI:
10.7554/eLife.28412.003
DOI:
10.7554/eLife.28412.004
DOI:
10.7554/eLife.28412.005
DOI:
10.7554/eLife.28412.006
DOI:
10.7554/eLife.28412.007
DOI:
10.7554/eLife.28412.008
DOI:
10.7554/eLife.28412.009
DOI:
10.7554/eLife.28412.010
DOI:
10.7554/eLife.28412.011
DOI:
10.7554/eLife.28412.012
DOI:
10.7554/eLife.28412.013
DOI:
10.7554/eLife.28412.014
DOI:
10.7554/eLife.28412.015
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2017
detail.hit.zdb_id:
2687154-3
