Research Topic

Contribution of Astrocyte-dependent Control of Synaptic Strength in Cognitive Functioning

About this Research Topic

The computational processes of the brain have long been considered to lie within neuronal networks, in which spike-time-dependent synaptic plasticity represents the cellular basis if learning and memory. Thus, synaptic plasticity, suggested to stem from a dialogue between genes and synapses, shaping the genesis and maintenance of dendritic arborization, has long been considered a neuronal process, supported by the metabolic function of astrocytes. However, converging evidence now acknowledges that astrocytes not only control synaptic homeostasis, which influences synaptic plasticity, but also contribute to information processing, signal transmission and regulation of neuronal excitability. Thus, the astrocyte network which sheathes billions of synapses indeed offer an uninterrupted supply of energy substrates, but also contributes to short-term plasticity by modulating neurotransmitter release from nearby presynaptic elements, and by activating postsynaptic glutamate receptors. In such three-sided (tripartite) synaptic organization, in which astrocytes are essential partners of the chemical synapse, astrocytes sense synaptic activity through a broad variety of ion channels, transporters and receptors expressed on their surface. Thus, astrocytes offer an activity-dependent contribution to the clearance of neurotransmitters (notably glutamate, and potentially dopamine in the striatum), thereby regulating cleft concentration and limiting diffusion to neighboring synapses, but they also, through calcium waves, release active substances to modulate synaptic strength in the many neurons with which they are in contact. Therefore, by synchronizing the neuronal activity, astrocytes bridge and influence neural circuits, and participate to the formation of complex neural ensembles that contribute to orchestrate plastic changes that ensure the stability and function of circuits. Because astrocytes tend to express the full portfolio of receptors that their neighboring neurons possess, their involvement in normal and abnormal cognitive and emotional processes remains to be understood.

This Research Topic aims to offer a new model of corticostriatal networks in which astrocytes are a key cellular component contributing to cognitive functioning, with an impetus on their contribution to stress- and drug-induced remodeling of synapses, thereby shaping long-term vulnerability to neurologic and psychiatric disorders.


Keywords: Astrocyte, synaptic plasticity, learning, cognition, gliotransmitter


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

The computational processes of the brain have long been considered to lie within neuronal networks, in which spike-time-dependent synaptic plasticity represents the cellular basis if learning and memory. Thus, synaptic plasticity, suggested to stem from a dialogue between genes and synapses, shaping the genesis and maintenance of dendritic arborization, has long been considered a neuronal process, supported by the metabolic function of astrocytes. However, converging evidence now acknowledges that astrocytes not only control synaptic homeostasis, which influences synaptic plasticity, but also contribute to information processing, signal transmission and regulation of neuronal excitability. Thus, the astrocyte network which sheathes billions of synapses indeed offer an uninterrupted supply of energy substrates, but also contributes to short-term plasticity by modulating neurotransmitter release from nearby presynaptic elements, and by activating postsynaptic glutamate receptors. In such three-sided (tripartite) synaptic organization, in which astrocytes are essential partners of the chemical synapse, astrocytes sense synaptic activity through a broad variety of ion channels, transporters and receptors expressed on their surface. Thus, astrocytes offer an activity-dependent contribution to the clearance of neurotransmitters (notably glutamate, and potentially dopamine in the striatum), thereby regulating cleft concentration and limiting diffusion to neighboring synapses, but they also, through calcium waves, release active substances to modulate synaptic strength in the many neurons with which they are in contact. Therefore, by synchronizing the neuronal activity, astrocytes bridge and influence neural circuits, and participate to the formation of complex neural ensembles that contribute to orchestrate plastic changes that ensure the stability and function of circuits. Because astrocytes tend to express the full portfolio of receptors that their neighboring neurons possess, their involvement in normal and abnormal cognitive and emotional processes remains to be understood.

This Research Topic aims to offer a new model of corticostriatal networks in which astrocytes are a key cellular component contributing to cognitive functioning, with an impetus on their contribution to stress- and drug-induced remodeling of synapses, thereby shaping long-term vulnerability to neurologic and psychiatric disorders.


Keywords: Astrocyte, synaptic plasticity, learning, cognition, gliotransmitter


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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31 January 2018 Manuscript

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Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

31 January 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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