For many years, our laboratory has been interested in the biobehavioral mechanisms of classical conditioning and, in particular, the mechanisms behind the conditioning, extinction, and inhibition of fear (e.g., Bouton, 1993, 2002, 2004). In fear conditioning, an organism learns to associate environmental stimuli with a frightening event, and those stimuli consequently evoke fear. Fear can be defined as a loosely coordinated set of physiological, behavioral, and cognitive responses that are designed to get the organism ready for a future aversive event.

Fear conditioning has long been thought to play a role in many anxiety disorders (e.g., Barlow, 2002; Bouton, Mineka, & Barlow, 2001; Mineka & Zinbarg, 1996). It is not difficult to see its relevance when humans are exposed to the type of very intense emotional trauma that can lead to posttraumatic stress disorder, or PTSD (e.g., Pitman, Shalev, & Orr, 2000). Thus, a combat veteran might associate the sound of a helicopter with a horrific battle experience, or a person involved in a collision with a train might associate the blast of the horn and the flash of the headlight with the trauma of the crash. When any of these cues is later encountered or imagined, it might therefore trigger a number of physiological and cognitive responses, the so-called “reexperiencing criteria” used in diagnosing PTSD (e.g., Pitman et al., 2000). And further, the facts that fear elicited this way can motivate avoidance behavior (e.g., Rescorla & Solomon, 1967) and engage analgesic responses (e.g., Bolles & Fanselow, 1980) presumably contribute to the diagnostic “avoidance/numbing” criteria.