Event:

Grey matter protoplasmic astrocytes extend numerous very thin processes and establish close contacts with thousands of neuronal synapses. For long time regarded little more than passive bystanders occupied with mere housekeeping activities, astrocytes have had a rampant career to become accepted players in brain development, neuronal excitability, plasticity and neurodegeneration.

A central element of these new roles for astrocytes is their capacity to read out neuronal activity and signal to neurons, via the release of neuroactive gliotransmitters at the tripartite synapse. However, the release mechanisms and even the very concept of calcium (Ca2+)-dependent gliotransmitter release from astrocytes continue being intensely debated. Despite intense work, no consensus has been reached, what astrocyte Ca2+ signal encode, and what are the downsteam signals that are triggered by them.

Studying astrocytes in their natural habitat 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 context, our work has faced some limitations of conventional methodologies. In response to these challenges, we have combined and developed novel tools for studying gliotransmission, from the molecular and single-vesicle level to cellular level in acute brain slices. I will talk about our work using total internal reflection fluorescence, single-vesicle spectroscopy, light-gated Ca2+ channels, and genetically encoded Ca2+ indicators to selectively read out and stimulate astrocyte activity.