1. Stress deficits in reward behaviour are associated with and replicated by dysregulated amygdala-nucleus accumbens pathway function in mice
- Author
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Madur, Lorraine, Ineichen, Christian, Bergamini, Giorgio, Greter, Alexandra, Poggi, Giulia, Cuomo-Haymour, Nagiua, Sigrist, Hannes, Sych, Yaroslav, Paterna, Jean-Charles, Bornemann, Klaus D, Viollet, Coralie, Fernandez-Albert, Francesc, Alanis-Lobato, Gregorio, Hengerer, Bastian, Pryce, Christopher R, and University of Zurich
- Subjects
10054 Clinic for Psychiatry, Psychotherapy, and Psychosomatics ,Medicine (miscellaneous) ,610 Medicine & health ,10064 Neuroscience Center Zurich ,Biological Sciences ,General Agricultural and Biological Sciences ,General Biochemistry, Genetics and Molecular Biology ,Neuroscience - Abstract
Reduced reward interest/learning and reward-to-effort valuation are distinct, common symptoms in neuropsychiatric disorders for which chronic stress is a major aetiological factor. Glutamate neurons in basal amygdala (BA) project to various regions including nucleus accumbens (NAc). The BA-NAc neural pathway is activated by reward and aversion, with many neurons being monovalent. In adult male mice, chronic social stress (CSS) leads to reduced discriminative reward learning (DRL) associated with decreased BA-NAc activity, and to reduced reward-to-effort valuation (REV) associated, in contrast, with increased BA-NAc activity. Chronic tetanus toxin BA-NAc inhibition replicates the CSS-DRL effect and causes a mild REV reduction, whilst chronic DREADDs BA-NAc activation replicates the CSS effect on REV without affecting DRL. This study provides evidence that stress disruption of reward processing involves the BA-NAc neural pathway; the bi-directional effects implicate opposite activity changes in reward (learning) neurons and aversion (effort) neurons in the BA-NAc pathway following chronic stress., Communications Biology, 6 (1), ISSN:2399-3642
- Published
- 2023