In:
eLife, eLife Sciences Publications, Ltd, Vol. 5 ( 2016-03-15)
Abstract:
Brain activity depends on the communication between neurons. This process takes place at the junctions between neurons, which are known as synapses, and typically involves one of the cells releasing a chemical messenger that binds to receptors on the other cell. The binding triggers a cascade of events inside the recipient cell, including the production of new receptors and their insertion into the cell membrane. These changes strengthen the synapse and are thought to be one of the ways in which the brain establishes and maintains memories. However, in order to induce these changes at the synapse, neurons must be able to activate the genes that encode their component parts. These genes are present inside the cell nucleus, which is located some distance away from the synapse. Studies have shown that signals can be sent from the nucleus to the synapse and vice versa, enabling the two parts of the cell to exchange information. Synapses that communicate using a chemical called glutamate have been particularly well studied; but it still remains unclear how the activation of receptors at these “glutamatergic synapses” is linked to activation of genes inside the nucleus at the molecular level. Dinamarca, Guzzetti et al. have now discovered that this process at glutamatergic synapses involves the movement of a protein messenger to the nucleus. Specifically, activation at synapses of a particularly common subtype of receptor, called NMDA, causes a protein called Ring Finger protein 10 (or RNF10 for short) to move from the synapse to the nucleus. To leave the synapse, RNF10 first has to bind to proteins called importins, which transport RNF10 into the nucleus. Once inside the nucleus, RNF10 binds to another protein that interacts with the DNA to start the production of new synaptic proteins. Further work is required to identify the molecular mechanisms that trigger RNF10 to leave the synapse. In addition, future studies should evaluate the levels and activity of RNF10 in brain disorders in which synapses are known to function abnormally.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.12430.001
DOI:
10.7554/eLife.12430.002
DOI:
10.7554/eLife.12430.003
DOI:
10.7554/eLife.12430.004
DOI:
10.7554/eLife.12430.005
DOI:
10.7554/eLife.12430.006
DOI:
10.7554/eLife.12430.007
DOI:
10.7554/eLife.12430.008
DOI:
10.7554/eLife.12430.009
DOI:
10.7554/eLife.12430.010
DOI:
10.7554/eLife.12430.011
DOI:
10.7554/eLife.12430.012
DOI:
10.7554/eLife.12430.013
DOI:
10.7554/eLife.12430.014
DOI:
10.7554/eLife.12430.015
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2016
detail.hit.zdb_id:
2687154-3
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