Terburg, DScheggia, DTriana del Rio, RKlumpers, FCiobanu, A.CMorgan, BMontoya, E.RBos, P.AGiobellina, Gvan den Burg, E.Hde Gelder, BStein, D.JStoop, Rvan Honk, J2025-01-042025-01-042018-10-18Terburg D, Scheggia D, Triana Del Rio R, Klumpers F, Ciobanu AC, Morgan B, Montoya ER, Bos PA, Giobellina G, van den Burg EH, de Gelder B, Stein DJ, Stoop R, van Honk J. The Basolateral Amygdala Is Essential for Rapid Escape: A Human and Rodent Study. Cell. 2018 Oct 18;175(3):723-735.e16. doi: 10.1016/j.cell.2018.09.028.10.1016/j.cell.2018.09.028https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6198024/https://doi.org/10.1016/j.cell.2018.09.028https://hdl.handle.net/11288/598059Rodent research delineates how the basolateral amygdala (BLA) and central amygdala (CeA) control defensive behaviors, but translation of these findings to humans is needed. Here, we compare humans with natural-selective bilateral BLA lesions to rats with a chemogenetically silenced BLA. We find, across species, an essential role for the BLA in the selection of active escape over passive freezing during exposure to imminent yet escapable threat (Timm). In response to Timm, BLA-damaged humans showed increased startle potentiation and BLA-silenced rats demonstrated increased startle potentiation, freezing, and reduced escape behavior as compared to controls. Neuroimaging in humans suggested that the BLA reduces passive defensive responses by inhibiting the brainstem via the CeA. Indeed, Timm conditioning potentiated BLA projections onto an inhibitory CeA pathway, and pharmacological activation of this pathway rescued deficient Timm responses in BLA-silenced rats. Our data reveal how the BLA, via the CeA, adaptively regulates escape behavior from imminent threat and that this mechanism is evolutionary conserved across rodents and humans.en© 2018 The Authors. Published by Elsevier Inc.https://www.elsevier.com/tdm/userlicense/1.0/articleS0092867418312406