New tools for investigating astrocyte-to-neuron communication

This is probably useful for determining how a neuron recruits a neighbor to help with a task, neuroplasticity in action.
http://www.frontiersin.org/Journal/10.3389/fncel.2013.00193/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w46-2013
Dongdong Li¹, Cendra Agulhon², Elke Schmidt¹, Martin Oheim¹ and Nicole Ropert^1*

• ¹Biophysics of Gliotransmitter Release Team, Laboratory of Neurophysiology and New Microscopies, INSERM U603, CNRS UMR 8154, University Paris Descartes, Paris, France
• ²Glia-Glia and Glia-Neuron Interactions in Neurophysiopathology Team, Laboratory of Neurophysiology and New Microscopies, INSERM U603, CNRS UMR 8154, University Paris Descartes, Paris, France

Gray matter protoplasmic astrocytes extend very thin processes and establish close contacts with synapses. It has been suggested that the release of neuroactive gliotransmitters at the tripartite synapse contributes to information processing. However, the concept of calcium (Ca²⁺)-dependent gliotransmitter release from astrocytes, and the release mechanisms are being debated. Studying astrocytes in their natural environment is challenging because: (i) astrocytes are electrically silent; (ii) astrocytes and neurons express an overlapping repertoire of transmembrane receptors; (iii) the size of astrocyte processes in contact with synapses are below the resolution of confocal and two-photon microscopes (iv) bulk-loading techniques using fluorescent Ca²⁺ indicators lack cellular specificity. In this review, we will discuss some limitations of conventional methodologies and highlight the interest of novel tools and approaches for studying gliotransmission. Genetically encoded Ca²⁺ indicators (GECIs), light-gated channels, and exogenous receptors are being developed to selectively read out and stimulate astrocyte activity. Our review discusses emerging perspectives on: (i) the complexity of astrocyte Ca²⁺ signaling revealed by GECIs; (ii) new pharmacogenetic and optogenetic approaches to activate specific Ca²⁺ signaling pathways in astrocytes; (iii) classical and new techniques to monitor vesicle fusion in cultured astrocytes; (iv) possible strategies to express specifically reporter genes in astrocytes.