Astrocytes were initially considered 'extras' in the brain, supporting neurons, the principal actors. But more recent work has suggested that they are involved in cognitive functions such as information processing, signal transmission, and neural and synaptic plasticity. Now these star-shaped cells are moving farther into the spotlight, as new research shows them to be essential in the formation of long-term memory.

Teams led by Cristina Alberini (Mount Sinai School of Medicine, New York, NY) and by Pierre Magistretti (Ecole Polytechnique Fédérale de Lausanne and University of Lausanne-CHUV, Switzerland) collaborated on the studies, which examined hippocampal changes and activities in rats exposed to foot shocks as a model of memory formation. Study development was driven by previous work indicating that learning increased the number of astrocytes in rat brains and that memory in a bead-discrimination exercise in young chicks required glycogenolysis, a process that occurs in astrocytes but not neurons.

Despite this evidence, however, identification and understanding of the mechanisms underlying astrocytes' contribution to cognitive functions is lacking. One such mechanism may be metabolic coupling, in which glycogen is broken down by astrocytes to produce lactate, which is transported to neurons to supply energy to meet the metabolic demands of memory formation. Long-term memory, in particular, has high energy demands, as it requires the activation of a cascade of genes and corresponding protein synthesis.

Alberini and Magistretti describe the astrocyte–neuron interaction in an article published in Cell (144, 810–823; 2011). They report that learning resulted in an increase in levels of lactate, derived from glycogen in astrocytes, in the rat hippocampus. Lactate release was essential for formation of long-term memory but not short-term memory. Lactate transport from astrocytes to neurons was also essential for long-term, but not short-term, memory formation: disrupting either the astrocytic or neuronal lactate transporters resulted in amnesia. The amnesia resulting from dysfunctional lactate release or astrocytic transport could be rescued by delivering lactate directly to the rats' brains; however, amnesia resulting from defects in the neuronal lactate transporter could not be rescued by lactate delivery.

The authors conclude that learning leads to astrocytic glycogenolysis and lactate release, and that subsequent astrocyte–neuron lactate transport is essential for long-term memory formation.

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Alberini and Magistretti's work helps to shed light on memory formation and may also aid in our understanding and ability to treat memory deficits associated with aging, dementia and neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.