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Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release
Dendritic spines are the major transmitter reception compartments of glutamatergic synapses in most principal neurons of the mammalian brain and play a key role in the function of nerve cell circuits. The formation of functional spine synapses is thought to be critically dependent on presynaptic glu...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cell Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5418202/ https://www.ncbi.nlm.nih.gov/pubmed/28426965 http://dx.doi.org/10.1016/j.neuron.2017.03.029 |
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author | Sigler, Albrecht Oh, Won Chan Imig, Cordelia Altas, Bekir Kawabe, Hiroshi Cooper, Benjamin H. Kwon, Hyung-Bae Rhee, Jeong-Seop Brose, Nils |
author_facet | Sigler, Albrecht Oh, Won Chan Imig, Cordelia Altas, Bekir Kawabe, Hiroshi Cooper, Benjamin H. Kwon, Hyung-Bae Rhee, Jeong-Seop Brose, Nils |
author_sort | Sigler, Albrecht |
collection | PubMed |
description | Dendritic spines are the major transmitter reception compartments of glutamatergic synapses in most principal neurons of the mammalian brain and play a key role in the function of nerve cell circuits. The formation of functional spine synapses is thought to be critically dependent on presynaptic glutamatergic signaling. By analyzing CA1 pyramidal neurons in mutant hippocampal slice cultures that are essentially devoid of presynaptic transmitter release, we demonstrate that the formation and maintenance of dendrites and functional spines are independent of synaptic glutamate release. |
format | Online Article Text |
id | pubmed-5418202 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Cell Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-54182022017-05-10 Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release Sigler, Albrecht Oh, Won Chan Imig, Cordelia Altas, Bekir Kawabe, Hiroshi Cooper, Benjamin H. Kwon, Hyung-Bae Rhee, Jeong-Seop Brose, Nils Neuron Report Dendritic spines are the major transmitter reception compartments of glutamatergic synapses in most principal neurons of the mammalian brain and play a key role in the function of nerve cell circuits. The formation of functional spine synapses is thought to be critically dependent on presynaptic glutamatergic signaling. By analyzing CA1 pyramidal neurons in mutant hippocampal slice cultures that are essentially devoid of presynaptic transmitter release, we demonstrate that the formation and maintenance of dendrites and functional spines are independent of synaptic glutamate release. Cell Press 2017-04-19 /pmc/articles/PMC5418202/ /pubmed/28426965 http://dx.doi.org/10.1016/j.neuron.2017.03.029 Text en © 2017 The Authors. Published by Elsevier Inc. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Report Sigler, Albrecht Oh, Won Chan Imig, Cordelia Altas, Bekir Kawabe, Hiroshi Cooper, Benjamin H. Kwon, Hyung-Bae Rhee, Jeong-Seop Brose, Nils Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release |
title | Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release |
title_full | Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release |
title_fullStr | Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release |
title_full_unstemmed | Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release |
title_short | Formation and Maintenance of Functional Spines in the Absence of Presynaptic Glutamate Release |
title_sort | formation and maintenance of functional spines in the absence of presynaptic glutamate release |
topic | Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5418202/ https://www.ncbi.nlm.nih.gov/pubmed/28426965 http://dx.doi.org/10.1016/j.neuron.2017.03.029 |
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