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Cell Rep. 2019 Jan 22;26(4):1010-1020.e5. doi: 10.1016/j.celrep.2018.12.105.

Plasticity at Thalamo-amygdala Synapses Regulates Cocaine-Cue Memory Formation and Extinction.

Author information

1
Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15213, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA; Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA 15213, USA.
2
Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15213, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.
3
Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15213, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA. Electronic address: torregrossam@upmc.edu.

Abstract

Repeated drug use has long-lasting effects on plasticity throughout the brain's reward and memory systems. Environmental cues that are associated with drugs of abuse can elicit craving and relapse, but the neural circuits responsible for driving drug-cue-related behaviors have not been well delineated, creating a hurdle for the development of effective relapse prevention therapies. In this study, we used a cocaine+cue self-administration paradigm followed by cue re-exposure to establish that the strength of the drug cue association corresponds to the strength of synapses between the medial geniculate nucleus (MGN) of the thalamus and the lateral amygdala (LA). Furthermore, we demonstrate, via optogenetically induced LTD of MGN-LA synapses, that reversing cocaine-induced potentiation of this pathway is sufficient to inhibit cue-induced relapse-like behavior.

KEYWORDS:

addiction; amygdala; cocaine; cue-induced reinstatement; extinction; memory; reconsolidation; relapse; thalamus

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