Reconstruction of great auk population dynamics suggests that hunting pressure alone could have been responsible for their extinction, demonstrating that even abundant, widespread species can be vulnerable to intense exploitation.

Dopamine signaling is necessary for normal fear extinction learning.

One-quarter of the Chondrichthyes have an elevated risk of extinction, mainly as a result of overfishing.

Prefrontal dopamine regulates inhibition of fear extinction circuits in the infralimbic cortex and disinhibition of fear expression circuits in the amygdala, leading to fear reinstatement.

There is no relationship between the demographic susceptibility to extinction and the estimated extinction chronology among Sahul’s megafauna, suggesting that human choices, a species’ ecological requirements, and/or random climate variation instead determined the extinction chronology.

Murine behavioral testing and biochemical experiments reveal AKT isoform- and sex-dependent mechanisms regulating affective behavior, memory formation, and extinction.

Insulin-like growth factor-1 activates the prefrontal cortex and improves the extinction of aversive memories.

Dopamine neurons in medial versus lateral VTA encode different signals during fear extinction, yet inhibition of both populations influences fear extinction, at different times.

Large-scale imaging analysis of CA1 reveals that distinct neural networks are involved in trace conditioning versus extinction learning, shedding light on how the hippocampus encodes different types of memory.

When the fear-enhancing effects of prior exposure to stress are absent, the expression of fear reflects normal neural activity in the medial prefrontal cortex, not stress-induced hyperactivity in the amygdala.