Astrocyte-neuron interaction at tripartite synapses

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Astrocyte-neuron interaction at tripartite synapses. / Araque, Alfonso; Perez-Alvarez, Alberto.

In: CURR DRUG TARGETS, Vol. 14, No. 11, 01.10.2013, p. 1220-1224.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

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@article{d5d770ec33d14d37bed381a0adfea911,
title = "Astrocyte-neuron interaction at tripartite synapses",
abstract = "Astrocytes, classically considered as supportive cells for neurons without a direct role in brain information processing, are emerging as relevant elements in brain physiology through their ability to regulate neuronal activity and synaptic transmission and plasticity. In relation to the key role of astrocyte-neuron interactions in synaptic physiology, accumulating evidence suggests that dysfunctions of neuron-astrocyte signaling may be linked to the pathology of various neurological and neurodegenerative diseases. In this article, we summarize the evidence supporting the importance of astrocyte-neuron communication in synaptic physiology, which have led to reveal astrocytes as integral elements of synaptic function. We also discuss how this novel view of astrocytic functions on brain physiology is prompting us to reconsider the possible astrocytic roles in brain diseases, and specifically in depression.",
keywords = "Animals, Astrocytes, Brain, Cell Communication, Humans, Mood Disorders, Neurons, Neurotransmitter Agents, Synapses, Synaptic Transmission",
author = "Alfonso Araque and Alberto Perez-Alvarez",
year = "2013",
month = oct,
day = "1",
doi = "10.2174/13894501113149990203",
language = "English",
volume = "14",
pages = "1220--1224",
journal = "CURR DRUG TARGETS",
issn = "1389-4501",
publisher = "Bentham Science Publishers B.V.",
number = "11",

}

RIS

TY - JOUR

T1 - Astrocyte-neuron interaction at tripartite synapses

AU - Araque, Alfonso

AU - Perez-Alvarez, Alberto

PY - 2013/10/1

Y1 - 2013/10/1

N2 - Astrocytes, classically considered as supportive cells for neurons without a direct role in brain information processing, are emerging as relevant elements in brain physiology through their ability to regulate neuronal activity and synaptic transmission and plasticity. In relation to the key role of astrocyte-neuron interactions in synaptic physiology, accumulating evidence suggests that dysfunctions of neuron-astrocyte signaling may be linked to the pathology of various neurological and neurodegenerative diseases. In this article, we summarize the evidence supporting the importance of astrocyte-neuron communication in synaptic physiology, which have led to reveal astrocytes as integral elements of synaptic function. We also discuss how this novel view of astrocytic functions on brain physiology is prompting us to reconsider the possible astrocytic roles in brain diseases, and specifically in depression.

AB - Astrocytes, classically considered as supportive cells for neurons without a direct role in brain information processing, are emerging as relevant elements in brain physiology through their ability to regulate neuronal activity and synaptic transmission and plasticity. In relation to the key role of astrocyte-neuron interactions in synaptic physiology, accumulating evidence suggests that dysfunctions of neuron-astrocyte signaling may be linked to the pathology of various neurological and neurodegenerative diseases. In this article, we summarize the evidence supporting the importance of astrocyte-neuron communication in synaptic physiology, which have led to reveal astrocytes as integral elements of synaptic function. We also discuss how this novel view of astrocytic functions on brain physiology is prompting us to reconsider the possible astrocytic roles in brain diseases, and specifically in depression.

KW - Animals

KW - Astrocytes

KW - Brain

KW - Cell Communication

KW - Humans

KW - Mood Disorders

KW - Neurons

KW - Neurotransmitter Agents

KW - Synapses

KW - Synaptic Transmission

U2 - 10.2174/13894501113149990203

DO - 10.2174/13894501113149990203

M3 - SCORING: Journal article

C2 - 23621508

VL - 14

SP - 1220

EP - 1224

JO - CURR DRUG TARGETS

JF - CURR DRUG TARGETS

SN - 1389-4501

IS - 11

ER -