Hippocampus and amygdala fear memory engrams re-emerge after contextual fear relapse.

Autor: Zaki Y; Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA., Mau W; Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA., Cincotta C; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Monasterio A; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Odom E; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Doucette E; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Grella SL; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Merfeld E; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Shpokayte M; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA., Ramirez S; Department of Psychological and Brain Sciences, Boston University, Boston, MA, 02215, USA. dvsteve@bu.edu.
Jazyk: angličtina
Zdroj: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology [Neuropsychopharmacology] 2022 Oct; Vol. 47 (11), pp. 1992-2001. Date of Electronic Publication: 2022 Aug 08.
DOI: 10.1038/s41386-022-01407-0
Abstrakt: The formation and extinction of fear memories represent two forms of learning that each engage the hippocampus and amygdala. How cell populations in these areas contribute to fear relapse, however, remains unclear. Here, we demonstrate that, in male mice, cells active during fear conditioning in the dentate gyrus of hippocampus exhibit decreased activity during extinction and are re-engaged after contextual fear relapse. In vivo calcium imaging reveals that relapse drives population dynamics in the basolateral amygdala to revert to a network state similar to the state present during fear conditioning. Finally, we find that optogenetic inactivation of neuronal ensembles active during fear conditioning in either the hippocampus or amygdala is sufficient to disrupt fear expression after relapse, while optogenetic stimulation of these same ensembles after extinction is insufficient to artificially mimic fear relapse. These results suggest that fear relapse triggers a partial re-emergence of the original fear memory representation, providing new insight into the neural substrates of fear relapse.
(© 2022. The Author(s), under exclusive licence to American College of Neuropsychopharmacology.)
Databáze: MEDLINE
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