Lesuis Sylvie L, Park Sungmo, Hoorn Annelies, Rashid Asim J, Mocle Andrew J, Salter Eric W, Vislavski Stefan, Gray Madison T, Torelli Angelica M, DeCristofaro Antonietta, Driever Wouter P F, van der Stelt Mario, Zweifel Larry S, Collingridge Graham L, Lefebvre Julie L, Walters Brandon J, Frankland Paul W, Hill Matthew N, Josselyn Sheena A
Program in Neurosciences & Mental Health, Hospital for Sick Children, 555 University Ave., Toronto, ON M5G 1X8, Canada; Cellular and Computational Neuroscience, Swammerdam Institute for Life Science, Amsterdam Neuroscience, University of Amsterdam, 1090 GE Amsterdam, the Netherlands.
Program in Neurosciences & Mental Health, Hospital for Sick Children, 555 University Ave., Toronto, ON M5G 1X8, Canada.
Cell. 2025 Jan 9;188(1):121-140.e20. doi: 10.1016/j.cell.2024.10.034. Epub 2024 Nov 15.
Stress induces aversive memory overgeneralization, a hallmark of many psychiatric disorders. Memories are encoded by a sparse ensemble of neurons active during an event (an engram ensemble). We examined the molecular and circuit processes mediating stress-induced threat memory overgeneralization in mice. Stress, acting via corticosterone, increased the density of engram ensembles supporting a threat memory in lateral amygdala, and this engram ensemble was reactivated by both specific and non-specific retrieval cues (generalized threat memory). Furthermore, we identified a critical role for endocannabinoids, acting retrogradely on parvalbumin-positive (PV+) lateral amygdala interneurons in the formation of a less-sparse engram and memory generalization induced by stress. Glucocorticoid receptor antagonists, endocannabinoid synthesis inhibitors, increasing PV+ neuronal activity, and knocking down cannabinoid receptors in lateral amygdala PV+ neurons restored threat memory specificity and a sparse engram in stressed mice. These findings offer insights into stress-induced memory alterations, providing potential therapeutic avenues for stress-related disorders.
应激会诱发厌恶记忆过度泛化,这是许多精神疾病的一个标志。记忆是由事件发生期间活跃的稀疏神经元集合(记忆痕迹集合)编码的。我们研究了介导小鼠应激诱导的威胁记忆过度泛化的分子和神经回路过程。应激通过皮质酮起作用,增加了杏仁核外侧支持威胁记忆的记忆痕迹集合的密度,并且这个记忆痕迹集合会被特定和非特定的检索线索重新激活(泛化威胁记忆)。此外,我们确定了内源性大麻素的关键作用,其逆向作用于小白蛋白阳性(PV+)杏仁核外侧中间神经元,参与应激诱导的形成较不稀疏的记忆痕迹和记忆泛化过程。糖皮质激素受体拮抗剂、内源性大麻素合成抑制剂、增加PV+神经元活性以及敲除杏仁核外侧PV+神经元中的大麻素受体,可恢复应激小鼠的威胁记忆特异性和稀疏的记忆痕迹。这些发现为应激诱导的记忆改变提供了见解,为应激相关疾病提供了潜在的治疗途径。