Astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses but not with synaptic strength

Honsek, Silke D.; Walz, Corinna; Kafitz, Karl W.; Rose, Christine R.

doi:10.1002/hipo.20843

Cited by 35 publications

(26 citation statements)

References 73 publications

(117 reference statements)

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“…Temporoammonic synapses are associated with theta oscillations and late-phase LTP and long-term memory consolidation [39-41]. In addition, astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses [42], demonstrating the direct participation of astrocytes in the hippocampal circuits that are involved in spatial memory. The presence of synaptic potentiation has been described previously to occur via astrocytic glutamate exocytosis at the entorhinal-to-dentate granular cells (the perforant pathway) [43,44] and Schaffer collaterals [45].…”

Section: Discussionmentioning

confidence: 99%

Spatial memory decline after masticatory deprivation and aging is associated with altered laminar distribution of CA1 astrocytes

et al. 2012

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BackgroundChewing imbalances are associated with neurodegeneration and are risk factors for senile dementia in humans and memory deficits in experimental animals. We investigated the impact of long-term reduced mastication on spatial memory in young, mature and aged female albino Swiss mice by stereological analysis of the laminar distribution of CA1 astrocytes. A soft diet (SD) was used to reduce mastication in the experimental group, whereas the control group was fed a hard diet (HD). Assays were performed in 3-, 6- and 18-month-old SD and HD mice.ResultsEating a SD variably affected the number of astrocytes in the CA1 hippocampal field, and SD mice performed worse on water maze memory tests than HD mice. Three-month-old mice in both groups could remember/find a hidden platform in the water maze. However, 6-month-old SD mice, but not HD mice, exhibited significant spatial memory dysfunction. Both SD and HD 18-month-old mice showed spatial memory decline. Older SD mice had astrocyte hyperplasia in the strata pyramidale and oriens compared to 6-month-old mice. Aging induced astrocyte hypoplasia at 18 months in the lacunosum-moleculare layer of HD mice.ConclusionsTaken together, these results suggest that the impaired spatial learning and memory induced by masticatory deprivation and aging may be associated with altered astrocyte laminar distribution and number in the CA1 hippocampal field. The underlying molecular mechanisms are unknown and merit further investigation.

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Section: Discussionmentioning

confidence: 99%

Spatial memory decline after masticatory deprivation and aging is associated with altered laminar distribution of CA1 astrocytes

et al. 2012

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“…In this way, activity in one astrocyte could spread through a network of neighboring astrocytes. However, either trains of sustained stimulation of synaptic activity (Grosche et al, 1999; Matyash et al, 2001) or a large number of activated fibers (Honsek et al, 2012) are necessary to induce this type of astrocytic Ca 2+ activity. In vivo it has been suggested that astrocytes can synchronize their activity in clusters of 2–5 astrocytes (Hirase et al, 2004; Sasaki et al, 2011a) or spread through a network consisting of dozens to hundreds of astrocytes (Hoogland et al, 2009; Nimmerjahn et al, 2009; Kuga et al, 2011).…”

Section: The Spatiotemporal Characteristics Of Astrocytic Ca2+ Signalsmentioning

confidence: 99%

The computational power of astrocyte mediated synaptic plasticity

Min¹,

Santello²,

Nevian³

2012

Front. Comput. Neurosci.

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Research in the last two decades has made clear that astrocytes play a crucial role in the brain beyond their functions in energy metabolism and homeostasis. Many studies have shown that astrocytes can dynamically modulate neuronal excitability and synaptic plasticity, and might participate in higher brain functions like learning and memory. With the plethora of astrocyte mediated signaling processes described in the literature today, the current challenge is to identify, which of these processes happen under what physiological condition, and how this shapes information processing and, ultimately, behavior. To answer these questions will require a combination of advanced physiological, genetical, and behavioral experiments. Additionally, mathematical modeling will prove crucial for testing predictions on the possible functions of astrocytes in neuronal networks, and to generate novel ideas as to how astrocytes can contribute to the complexity of the brain. Here, we aim to provide an outline of how astrocytes can interact with neurons. We do this by reviewing recent experimental literature on astrocyte-neuron interactions, discussing the dynamic effects of astrocytes on neuronal excitability and short- and long-term synaptic plasticity. Finally, we will outline the potential computational functions that astrocyte-neuron interactions can serve in the brain. We will discuss how astrocytes could govern metaplasticity in the brain, how they might organize the clustering of synaptic inputs, and how they could function as memory elements for neuronal activity. We conclude that astrocytes can enhance the computational power of neuronal networks in previously unexpected ways.

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“…A number of studies in situ and in vivo has established strong evidence for neuron-to-astrocyte signaling in the brain [1]–[6]. While a primary target of synaptically-released neurotransmitter is ionotropic receptors in the postsynaptic membrane to produce shifts in neuronal membrane potential, neurotransmitter can spill out of the synapse to stimulate Gq G protein-coupled (metabotropic) receptors (Gq GPCRs) on perisynaptic astrocyte processes [1]–[6].…”

Section: Introductionmentioning

confidence: 99%

Bidirectional Scaling of Astrocytic Metabotropic Glutamate Receptor Signaling following Long-Term Changes in Neuronal Firing Rates

Xie

Sun²,

Murphy³

et al. 2012

PLoS ONE

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Very little is known about the ability of astrocytic receptors to exhibit plasticity as a result of changes in neuronal activity. Here we provide evidence for bidirectional scaling of astrocytic group I metabotropic glutamate receptor signaling in acute mouse hippocampal slices following long-term changes in neuronal firing rates. Plasticity of astrocytic mGluRs was measured by recording spontaneous and evoked Ca2+ elevations in both astrocytic somata and processes. An exogenous astrocytic Gq G protein-coupled receptor was resistant to scaling, suggesting that the alterations in astrocyte Ca2+ signaling result from changes in activity of the surface mGluRs rather than a change in intracellular G protein signaling molecules. These findings suggest that astrocytes actively detect shifts in neuronal firing rates and adjust their receptor signaling accordingly. This type of long-term plasticity in astrocytes resembles neuronal homeostatic plasticity and might be important to ensure an optimal or expected level of input from neurons.

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Astrocyte calcium signals at Schaffer collateral to CA1 pyramidal cell synapses correlate with the number of activated synapses but not with synaptic strength

Cited by 35 publications

References 73 publications

Spatial memory decline after masticatory deprivation and aging is associated with altered laminar distribution of CA1 astrocytes

Spatial memory decline after masticatory deprivation and aging is associated with altered laminar distribution of CA1 astrocytes

The computational power of astrocyte mediated synaptic plasticity

Bidirectional Scaling of Astrocytic Metabotropic Glutamate Receptor Signaling following Long-Term Changes in Neuronal Firing Rates

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