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

46 Pages Posted: 26 Feb 2019 Publication Status: Published

See all articles by Matthew T. Rich

Matthew T. Rich

University of Pittsburgh - Department of Psychology

Yanhua H. Huang

University of Pittsburgh - Department of Psychology

Mary M. Torregrossa

University of Pittsburgh - Department of Psychology

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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 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 cocaineinduced potentiation of this pathway is sufficient to inhibit cue-induced relapse-like behavior.

Suggested Citation

Rich, Matthew T. and Huang, Yanhua H. and Torregrossa, Mary M., Plasticity at Thalamo-Amygdala Synapses Regulates Cocaine-Cue Memory Formation and Extinction (2018). Available at SSRN: https://ssrn.com/abstract=3205405 or http://dx.doi.org/10.2139/ssrn.3205405
This version of the paper has not been formally peer reviewed.

Matthew T. Rich

University of Pittsburgh - Department of Psychology

United States

Yanhua H. Huang

University of Pittsburgh - Department of Psychology

United States

Mary M. Torregrossa (Contact Author)

University of Pittsburgh - Department of Psychology ( email )

United States

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