Who Needs Emotions? The Brain Meets the Robot

asic principles for emotional processing 93
to increases in amygdala activity, as measured by fMRI (LaBar et al., 1998;
Buchel & Dolan, 2000), and these effects also occur to subliminal stimuli
(Morris et al., 1999). Additionally, when the activity of the amygdala during
fear conditioning is cross-correlated with the activity in other regions of
the brain, the strongest relations are seen with subcortical (thalamic and
collicular) rather than cortical areas, further emphasizing the importance of
the direct thalamic–amygdala pathway in the human brain (Morris, Ohman,
& Dolan, 1999). Work in humans has further implicated the amygdala in
social interactions (Hart et al., 2000; Phelps et al., 2000). Other aspects of
emotion and the human brain are reviewed elsewhere (Davidson & Irwin,
1999; Critchley, Mathias, & Dolan, 2002; Dolan & Vuilleumier, 2003).
There is growing enthusiasm for the notion that fear-learning processes
similar to those occurring in fear-conditioning experiments might indeed be
an important factor in certain human anxiety disorders. For example, fearconditioning
models of posttraumatic stress disorder (PTSD) and panic disorder
(Goddard & Charney, 1997; Rauch et al., 2000) have been proposed
by researchers in these fields.
Earlier in the 20th century, the notion that conditioned fear contributes
to phobias and related fear disorders was fairly popular. However, this idea
fell out of favor because laboratory fear conditioning seemed to produce easily
extinguishable fear, whereas clinical fear is difficult to treat. Fear disorders
involve a special kind of learning, called “prepared learning,” where the CS
is biologically significant rather than neutral (de Silva, Rachman, & Seligman,
1977; Ohman, 1992). While preparedness may indeed contribute, there is
another factor to consider. In studies of rats, easily extinguished fear could
be converted into difficult to extinguish fear with damage to the medial
prefrontal cortex (Morgan, Romanski, & LeDoux, 1993). This suggested that
alterations in the organization of the medial prefrontal regions might predispose
certain people in some circumstances (e.g., stressful situations) to
learn in a way that is difficult to extinguish (treat) under normal circumstances.
These changes could come about because of genetic or experiential
factors or some combination. Recent imaging studies have shown amygdala
alterations in PTSD, panic disorders, and depression (Price, 1999; Davidson,
Pizzagalli, Nitschke, & Putnam, 2002; Anand & Shekhar, 2003; Drevets,
2003; Rauch, Shin, & Wright, 2003; Wright et al., 2003).
One of the key issues for the coming years is to integrate research on
emotion and cognition. As a step in this direction, we consider how fear
processing by the amygdala is influenced by and can influence the perceptual,
attentional, and memory functions of the cortex.
The amygdala receives inputs from cortical sensory-processing regions
of each sensory modality and projects back to these as well (Amaral, Price,
Pitkanen, & Carmichael, 1992; McDonald, 1998). These projections allow