The nature and distribution of the synaptic changes that underlie memory are not well understood. Here we examine the synaptic plasticity behind context fear conditioning in male and female mice and find that new learning produces synaptic potentiation specifically onto engram neurons in the basolateral amygdala. This potentiation lasts at least 7 days, is reversed by extinction, and its disruption impairs memory recall. High frequency optogenetic stimulation of the CS and US-activated ensembles, or biochemical induction of synaptic potentiation in US-responsive neurons alone, is sufficient to produce a context fear association without prior associative training. These results suggest that plasticity of CS inputs onto US-responsive amygdala neurons underlies memory formation and is necessary and sufficient to establish context fear associations.

© 2025. The Author(s).

记忆背后突触变化的性质和分布尚不完全清楚。在这里，我们研究了雄性和雌性小鼠在情境恐惧条件作用中的突触可塑性，并发现新的学习会产生特定于基底外侧杏仁核中印记神经元上的突触强化。这种强化至少可以持续7天，在消退过程中会被逆转，其破坏会损害记忆回忆。高频光遗传学刺激CS和US激活的集合体，或在仅响应US的神经元上生化诱导突触增强，足以在没有先前联想训练的情况下产生情境恐惧关联。这些结果表明，CS输入到响应US的杏仁核神经元上的可塑性是记忆形成的基础，并且对于建立情境恐惧联系而言既是必要的也是充分的。

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