Metabolic crosstalk between neurons and astrocytes: Energetic consequences of sodium homeostasis perturbation in astrocytes
The brain accounts for about 20% of the total body glucose consumption. Furthermore, a tight link exists between the level of local electrical activity of neuronal circuits and the local consumption of energy equivalents. Astrocytes have been shown to play a central role in the regulation of this so-called neurometabolic coupling. The main focus of our research is to tackle the interactions between astrocytes and neurons at the level of energy metabolism. Glutamate released from neurons in the synaptic cleft during activity is removed mainly by surrounding astrocytes by co-transport with sodium ions. The resulting sodium increase in astrocytes triggers a cascade of signaling events that is thought to lead to the delivery of energy equivalents to neurons. In parallel with these metabolic functions, recent studies have shown that astrocytes express a form of non-electrical excitability, called calcium excitability. To gain access to spatial and temporal aspects of these dynamic interactions, we mainly use optical microscopy tools, in particular wide-field and confocal fluorescence microscopy, UV flash photolysis, and combine these approaches with electrophysiology. These studies have relevance to certain pathophysiological conditions, as alterations in brain energy metabolism have been observed for instance in several neurodegenerative diseases such as Alzheimer's disease. Interfering with key elements of neuron-glia interactions could potentially lead a better understanding of these diseases and to novel therapeutic strategies.
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