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Drug-induced synaptic plasticity : a key to addiction ?| old_uid | 5958 |
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| title | Drug-induced synaptic plasticity : a key to addiction ? |
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| start_date | 2009/01/12 |
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| schedule | 12h |
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| online | no |
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| location_info | Bât. André Lwoff, salle 14 |
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| summary | Over the last two decades much effort has been devoted to the study of long-term synaptic plasticity as a candidate mechanism underlying learning and memory. More recently dysfunctional synaptic plasticity has been implicated in several brain diseases, including addiction. While addictive substances invariably lead adaptive changes in the brain, only a fraction of subjects will eventually be diagnosed with the disease. Research is therefore aimed at dissecting the molecular and cellular mechanism that underlie these adaptive changes and asking how such changes may differ in addicted subjects. Our lab is focusing on the observation that addictive drugs evoke specific forms of synaptic plasticity, starting hours after a first exposure with an enhancement of the excitatory afferents on dopamine neurons in the VTA. This plasticity can be detected ex vivo in brain slices by measuring the AMPA/NMDA ratio and the rectification of evoked AMPAR-mediated synaptic currents. Recent data now suggest that the reversal of this plasticity in vivo depends on the activation of metabotropic glutamate receptors (mGluR1). Consistent with this idea, a stereotaxic injection of a TAT conjugated peptide that disruptions the interaction of mGluR1 and homer, significantly increases the persistence of the plasticity. We explore the consequences of the parsitance of the drug-evoked plasticity for other brain regions. |
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| responsibles | Granon |
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