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The oxytocin story keeps coming together. The papers by Guastella et al. and Domes et al. are merely the latest integrative chapters, and it strikes me that it may be time to stop the play-by-play for a “state of the amygdala, with special reference to oxytocin” talk. Here's what we know. The amygdala has two essential functions: Pavlovian and instrumental conditioning. The basolateral amygdala does the former: it associates previously unconditioned cues (e.g., your patient's face) with conditioned stimuli (dread) to assign negative or positive valence to the various stimuli you come across day to day. The amygdala's ideas about what is good (it's not just for fear anymore!) and bad aren't particularly sophisticated. Compared to the orbitofrontal cortex, with its highly nuanced and ever-changing assessments of what is good and bad and, most of all, what is grey, the amygdala is a ruffian: plebian, blunt, simple, direct. And once it makes its decision, it's not apt to change it. The basolateral amygdala then passes these associated stimuli, with their associated adaptive implications, along to the centromedial nucleus, which oversees operational conditioning of an autonomic sort: it's the centromedial that gets you ready for fight, flight, or neither. In between the two lie the intercalated nuclei, heavily GABAergic cell populations that essentially put the breaks on the automatic conversion of Pavlovian association (my dreaded patient!) to action (elevated heart rate, the urge to run). On top of this relatively simple system impinge a variety of neurotransmitter systems, including most importantly for psychiatr