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Plasticity of Neuron-Glial Transmission: Equipping Glia for Long-Term Integration of Network Activity.

Croft W, Dobson KL, Bellamy TC - Neural Plast. (2015)

Bottom Line: The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes.We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation.We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

View Article: PubMed Central - PubMed

Affiliation: School of Life Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK.

ABSTRACT
The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes. In recent years, glial cells (most notably astrocytes) have been recognized as active participants in the modulation of synaptic transmission and synaptic plasticity, implicating these electrically nonexcitable cells in information processing in the brain. While the concept of bidirectional communication between neurons and glia and the mechanisms by which gliotransmission can modulate neuronal function are well established, less attention has been focussed on the computational potential of neuron-glial transmission itself. In particular, whether neuron-glial transmission is itself subject to activity-dependent plasticity and what the computational properties of such plasticity might be has not been explored in detail. In this review, we summarize current examples of plasticity in neuron-glial transmission, in many brain regions and neurotransmitter pathways. We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation. We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

No MeSH data available.


Related in: MedlinePlus

Modes of neuron-glial transmission and plasticity. Summary of the routes for neuron-glial transmission in which long-term plasticity after electrical stimulation of presynaptic cells has been demonstrated. Left panel shows synaptic transmission for NG2 cells (analogous to classical neuronal LTP), middle panel shows ectopic transmission at cerebellar Bergmann glia, and right panel shows volume transmission through diffusion to extrasynaptic receptors. The table shows cell types, receptors, stimulation protocols, and forms of glial plasticity that have been described. See main text for references and further details.
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fig1: Modes of neuron-glial transmission and plasticity. Summary of the routes for neuron-glial transmission in which long-term plasticity after electrical stimulation of presynaptic cells has been demonstrated. Left panel shows synaptic transmission for NG2 cells (analogous to classical neuronal LTP), middle panel shows ectopic transmission at cerebellar Bergmann glia, and right panel shows volume transmission through diffusion to extrasynaptic receptors. The table shows cell types, receptors, stimulation protocols, and forms of glial plasticity that have been described. See main text for references and further details.

Mentions: The accumulating evidence for neuron-glial plasticity indicates that signal processing through these routes for transmission can be altered in an activity-dependent manner, suggesting that memory processes could be accommodated within the network. However, it is striking that the computational properties of glial plasticity differ from those typical for induction of synaptic plasticity. The canonical example of synaptic plasticity is hippocampal LTP [2], which is typically evoked by a brief, high-frequency tetanus. Thus, a stereotyped incident signal is able to induce a change in synaptic strength within seconds, which can subsequently last for hours (or even years [8]). In contrast, plasticity appears to arise from less temporally precise induction signals (Figure 1).


Plasticity of Neuron-Glial Transmission: Equipping Glia for Long-Term Integration of Network Activity.

Croft W, Dobson KL, Bellamy TC - Neural Plast. (2015)

Modes of neuron-glial transmission and plasticity. Summary of the routes for neuron-glial transmission in which long-term plasticity after electrical stimulation of presynaptic cells has been demonstrated. Left panel shows synaptic transmission for NG2 cells (analogous to classical neuronal LTP), middle panel shows ectopic transmission at cerebellar Bergmann glia, and right panel shows volume transmission through diffusion to extrasynaptic receptors. The table shows cell types, receptors, stimulation protocols, and forms of glial plasticity that have been described. See main text for references and further details.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4539116&req=5

fig1: Modes of neuron-glial transmission and plasticity. Summary of the routes for neuron-glial transmission in which long-term plasticity after electrical stimulation of presynaptic cells has been demonstrated. Left panel shows synaptic transmission for NG2 cells (analogous to classical neuronal LTP), middle panel shows ectopic transmission at cerebellar Bergmann glia, and right panel shows volume transmission through diffusion to extrasynaptic receptors. The table shows cell types, receptors, stimulation protocols, and forms of glial plasticity that have been described. See main text for references and further details.
Mentions: The accumulating evidence for neuron-glial plasticity indicates that signal processing through these routes for transmission can be altered in an activity-dependent manner, suggesting that memory processes could be accommodated within the network. However, it is striking that the computational properties of glial plasticity differ from those typical for induction of synaptic plasticity. The canonical example of synaptic plasticity is hippocampal LTP [2], which is typically evoked by a brief, high-frequency tetanus. Thus, a stereotyped incident signal is able to induce a change in synaptic strength within seconds, which can subsequently last for hours (or even years [8]). In contrast, plasticity appears to arise from less temporally precise induction signals (Figure 1).

Bottom Line: The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes.We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation.We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

View Article: PubMed Central - PubMed

Affiliation: School of Life Sciences, University of Nottingham Medical School, Nottingham NG7 2UH, UK.

ABSTRACT
The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes. In recent years, glial cells (most notably astrocytes) have been recognized as active participants in the modulation of synaptic transmission and synaptic plasticity, implicating these electrically nonexcitable cells in information processing in the brain. While the concept of bidirectional communication between neurons and glia and the mechanisms by which gliotransmission can modulate neuronal function are well established, less attention has been focussed on the computational potential of neuron-glial transmission itself. In particular, whether neuron-glial transmission is itself subject to activity-dependent plasticity and what the computational properties of such plasticity might be has not been explored in detail. In this review, we summarize current examples of plasticity in neuron-glial transmission, in many brain regions and neurotransmitter pathways. We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation. We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

No MeSH data available.


Related in: MedlinePlus