Abstract
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.
Highlights
A number of studies in situ and in vivo has established strong evidence for neuron-to-astrocyte signaling in the brain [1,2,3,4,5,6]
We set out to determine if longterm changes in CA3 neuron firing rates lead to long-term plasticity of spontaneous and evoked astrocytic Gq GPCR Ca2+ elevations in CA1 stratum radiatum (s.r.) astrocytes in acute hippocampal slices
Preparation of Acute Hippocampal Slices Acute slices were chosen for this study because the majority of the neuronal network and neuron-to-astrocyte communication remains intact in acute slices
Summary
A number of studies in situ and in vivo has established strong evidence for neuron-to-astrocyte signaling in the brain [1,2,3,4,5,6]. A number of specific changes in spontaneous and evoked Ca2+ elevations occur following manipulation of Gq GPCR expression levels in cultured cells. These include an increase in the percentage of cells in the population exhibiting spontaneous Ca2+ elevations [7,8,9], a higher response probability to agonist stimulation [10,11], and a decrease in Ca2+ response latency to agonist [10,11,12]. An exciting possibility is that astrocytic Gq GPCRs exhibit plasticity in response to changes in neuronal activity in situ. We set out to determine if longterm changes in CA3 neuron firing rates lead to long-term plasticity of spontaneous and evoked astrocytic Gq GPCR Ca2+ elevations in CA1 stratum radiatum (s.r.) astrocytes in acute hippocampal slices
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