11/ In summary, we identified novel signatures of stress resilience and susceptibility in the BLA, and could rescue these dysfunctional neural dynamics and anhedonia in susceptible mice by manipulating vCA1->BLA inputs.

10/ We found that spontaneous activity of susceptible mice had a greater number of distinct neural states in the BLA compared to controls. Notably, spontaneous activity was better at distinguishing between susceptible, resilient, and control mice than classic behavioral measures.

8/ Next, we modulated BLA activity by chemogenetic activation of the vCA1->BLA pathway. This rescued aberrant population dynamics and anhedonia-like behavior in susceptible mice, suggesting that targeting this pathway enhances BLA circuit function and rescues anhedonic behaviors.

7/ Are there neural representations that reflect the intention of mice to switch or stay on the same reward choice as the previous trial? Yes! But only in the BLA of susceptible mice, reminiscent of rumination-like states commonly observed in individuals with depression.

6/ We next examined the origins of anhedonic behavior in susceptible mice by analyzing the sequence of reward choices. We found that the choice sequence was Markovian, where the probability of choosing water or sucrose depends on the choice in the previous trial.

5/ We found enhanced reward choice (sucrose vs. water) representations at both single-neuron and population levels in the BLA of resilient mice as compared to controls and susceptible mice.

3/ We performed high-density Neuropixels recording in the basolateral amygdala (BLA) and ventral CA1 (vCA1) in mice following chronic social defeat stress while they performed a head-fixed sucrose preference task to assess anhedonia-like behavior.