Emotional reactions may come in many forms and have different causes. But one of the main responses is the fear response, which has been shown to involved the amygdala. Different nuclei of the amygdala may contribute differentially to the fear response process.
One vital feature of emotion and amygdala is that emotional responses can be reduced, and eventually diminish. This is one of the basic mechanisms at play when we habituate to (or even extinguish) fearful stimuli. But is is also possible to reduce fear responses through more controlled processes, what has been termed cognitive emotion regulation. Such basic cognitive mechanisms underlie the psychological treatment of, e.g., phobias. In other words, there are two ways of reducing fear responses of the amygdala: 1) through habituation/extinction and 2) through cognitive (“rational”?) processing.
However, the exact neurobiological nature of these processes have been unknown. In a recent paper in Neuron, authored by Mauricio Delgado, and including prominent emotion researchers such as Joseph LeDoux, Elisabeth Phelps, looks at precicely this relationship. Using an emotion regulation strategy, the researchers compared the brain mechanisms (using fMRI) for conditioned fear regulation and for classic extinction.
From the methods section, one can read:
Each trial began with the presentation of a word cue, presented for 2 s, which instructed the participant on the type of trial. It was followed by either a blue or yellow square that served as a conditioned stimulus (CS) and was presented for 4 s. A mild shock to the wrist served as the unconditioned stimulus (US) and was administered during the last 200 ms for six of the CS trials. During one experimental session, a specific colored square (e.g., blue) was paired with the US, thus serving as the CS+, while the other square (e.g., yellow) served as the CS−. This contingency was counterbalanced across participants. The trial concluded with a 12 s intertrial interval.
When instructed to “attend,” participants were asked to view the stimulus and attend to their natural feelings regarding which CS was presented. In these Attend trials, for example, participants might focus on the fact that they may receive a shock (if the cue was followed by a CS+) or would never receive a shock (if the cue was followed by a CS−). When instructed to “reappraise,” participants were asked to view the CS and try to imagine something in nature that was calming, prompted by the color of the CS. During these Regulation trials, for example, participants could think of an image of the ocean or a blue sky when viewing the blue square, or they could think of the sunshine or a field of daffodils when viewing the yellow square.
During both cases of fear reduction, the amygdala (red in top image) activation level went from high to low, for both What the researchers found was that during extinction learning, the ventromedial prefrontal cortex (orange in top) showed a higher activity, and this was thought to cause the observed reduction in amygdala activation. In contrast, cognitive emotion control lead to a higher activation in the dorsolateral PfC (blue in top image).
So this is a very nice demonstration of two different mechanisms of emotion regulation. However, it stills seems open to me whether the two are overlapping or very different mechanisms. One way of assuming the relationship is that the dorsolateral PfC works through the ventromedial PfC on regulating the amygdala. However, it may also be possible that the dorsolateral PfC bypasses the ventromedial PfC altogether. By comparing the activation patterns of all three structures, the findings suggested that the dorsolateral PfC works on the amygdala through the ventromedial PfC. Or, as put by the authors:
Our results support a model in which the lateral PFC regions engaged by the online manipulation of information characteristic of cognitive emotion regulation strategies (for review see Ochsner and Gross, 2005) influences amygdala function through connections to vmPFC regions that are also thought to inhibit the amygdala during extinction (Milad and Quirk, 2002). These results are consistent with the suggestion that vmPFC may play a general regulatory role in diminishing fear across a range of paradigms (e.g., [Kim et al., 2003] and [Urry et al., 2006]).
The implications of these findings may be plenty, but a few immediately comes to mind: first, the identification of the dorsolateral PfC in controlling emotions may, in general, be used as a marker for emotional regulation in different psychological states. Lie detection may be one issue, and studies of implicit racism seem to suggest the same. Another interesting consequence is in the modelling of the phylogeny and ontogeny of emotion regulation in primates. The present results may suggest that the dorsolateral PfC role in emotion regulation has occurred later in primate evolution, and that it works through a more “ancient” ventromedial PfC basic regulation of the amygdala. It may even be possible that developmental studies can show that the later maturation of the dorsolateral PfC also corresponds to the development of emotional control. Finally, this idea may also serve as a good model for studying brain injury and the consequences of emotion regulation.