Articles by Alison X. Xie in JoVE
Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates Alison X. Xie1, Kelli Lauderdale1, Thomas Murphy1, Timothy L. Myers1, Todd A. Fiacco2,3 1Graduate Program in Neuroscience, University of California Riverside, 2Department of Cell Biology and Neuroscience, University of California Riverside, 3Center for Glial-Neuronal Interactions, University of California Riverside Here we describe an adaptation of protocols used to induce homeostatic plasticity in neurons for the study of plasticity of astrocytic G protein-coupled receptors. Recently used to examine changes in astrocytic group I mGluRs in juvenile mice, the method can be applied to measure scaling of various astrocytic GPCRs, in tissue from adult mice in situ and in vivo, and to gain a better appreciation of the sensitivity of astrocytic receptors to changes in neuronal activity.
Other articles by Alison X. Xie on PubMed
Modeling CNS Microglia: the Quest to Identify Predictive Models Drug Discovery Today. Disease Models. 2008 | Pubmed ID: 19444332 The mammalian central nervous system (CNS) is populated very early in development by tissue macrophages referred to as microglia. By adulthood, this CNS-resident population is found in all regions of the brain and spinal cord. Despite nearly a century of study, the in vivo function of microglia and the extent that they contribute to the onset, progression and recovery from neuroinflammatory disorders is still a subject of debate. Partly, the debate of whether activated microglia promote neuroprotection or neurodegeneration is fueled by the contrasting results derived from the different models used to assay microglial function. Here we discuss the strengths, weaknesses and utility of some of the most commonly used in vivo and in vitro models.
Bidirectional Scaling of Astrocytic Metabotropic Glutamate Receptor Signaling Following Long-term Changes in Neuronal Firing Rates PloS One. 2012 | Pubmed ID: 23166735 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.