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    Lactate release from astrocytes to neurons contributes to cocaine memory formation

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    Type
    Article
    Authors
    Boury-Jamot, Benjamin
    Halfon, Olivier
    Magistretti, Pierre J. cc
    Boutrel, Benjamin cc
    KAUST Department
    Biological and Environmental Sciences and Engineering (BESE) Division
    Bioscience Program
    Date
    2016-10-04
    Online Publication Date
    2016-10-04
    Print Publication Date
    2016-12
    Permanent link to this record
    http://hdl.handle.net/10754/622120
    
    Metadata
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    Abstract
    The identification of neural substrates underlying the long lasting debilitating impact of drug cues is critical for developing novel therapeutic tools. Metabolic coupling has long been considered a key mechanism through which astrocytes and neurons actively interact in response of neuronal activity, but recent findings suggested that disrupting metabolic coupling may represent an innovative approach to prevent memory formation, in particular drug-related memories. Here, we review converging evidence illustrating how memory and addiction share neural circuitry and molecular mechanisms implicating lactate-mediated metabolic coupling between astrocytes and neurons. With several aspects of addiction depending on mnemonic processes elicited by drug experience, disrupting lactate transport involved in the formation of a pathological learning, linking the incentive, and motivational effects of drugs with drug-conditioned stimuli represent a promising approach to encourage abstinence.
    Citation
    Boury-Jamot B, Halfon O, Magistretti PJ, Boutrel B (2016) Lactate release from astrocytes to neurons contributes to cocaine memory formation. BioEssays 38: 1266–1273. Available: http://dx.doi.org/10.1002/bies.201600118.
    Sponsors
    The financial support of the NCCR Synapsy and the Préfargier Foundation is gratefully acknowledged. The authors thank Jessica Scheurer (graphic designer at Lausanne University Hospital) for assistance in the preparation of the figures.
    Publisher
    Wiley
    Journal
    BioEssays
    DOI
    10.1002/bies.201600118
    Additional Links
    http://onlinelibrary.wiley.com/doi/10.1002/bies.201600118/abstract
    ae974a485f413a2113503eed53cd6c53
    10.1002/bies.201600118
    Scopus Count
    Collections
    Articles; Biological and Environmental Science and Engineering (BESE) Division; Bioscience Program

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