Who Needs Emotions? The Brain Meets the Robot

asic principles for emotional processing 95
cortex (Aston-Jones, Rajkowski, & Cohen, 2000; Kapp, Whalen, Supple, &
Pascoe, 1992; Weinberger, 1995; Holland & Gallagher, 1999). Thus, once
the amygdala detects danger, it can activate these arousal systems, which
can then influence sensory processing. The bodily responses initiated by the
amygdala can also influence cortical areas by way of feedback from either
proprioceptive or visceral signals or hormones (McGaugh et al., 1995;
Damasio, 1994). Amygdala regulation of the cortex by either direct or indirect
routes could facilitate the processing of stimuli that signal danger even
if such stimuli occur outside of the attentional field (Armony, Quirk, &
LeDoux, 1998).
The amygdala also interacts with areas within the medial prefrontal
cortex, a structure known to be involved in working memory. These areas
have widespread influences on cognition and behavior, but they also send
connections to several amygdala regions, including CE, as well as to brainstem
outputs of CE, allowing cognitive functions organized in prefrontal
regions, especially working memory, to regulate the amygdala and its fear
reactions (Fig. 4.4).
The amygdala is a collection of diverse nuclei. It thus should come as no
surprise that consequences of damage to this region vary, depending on where
the lesion is located (Garcia, Vouimba, Baudry, & Thompson, 1999; Morgan,
Schulkin, & LeDoux, 2003; Quirk & Gehlert, 2003; Rosenkranz & Grace,
2003). Some lesions led to a marked exaggeration of fear reactions, while
others did not. Overall, this work suggested that the prefrontal cortex and
amygdala are reciprocally related. That is, in order for the amygdala to respond
to fear, the prefrontal region has to be shut down. By the same logic,
when the prefrontal region is active, the amygdala would be inhibited, making
it harder to express fear. Pathological fear, then, may occur when the
amygdala is unchecked by the prefrontal cortex, and fear therapy may be a
process by which we learn to increase activity in the prefrontal region so
that the amygdala is less free to express fear. Clearly, decision-making ability
in emotional situations is impaired in humans with damage to the medial
prefrontal cortex (Damasio, 1994; Bechara, Damasio, & Damasio, 2003),
and abnormalities in the prefrontal cortex may predispose people to develop
fear and anxiety disorders. These abnormalities that bias one to develop
pathological fear could be due to genetic or epigenetic organization of medial
prefrontal synapses or to experiences that subtly alter medial prefrontal
synaptic connections. Indeed, the behavior of nonhuman animals with abnormalities
of the medial prefrontal cortex is reminiscent of humans with
anxiety disorders: they develop fear reactions that are difficult to regulate.
Objective information about the world may indicate that the situation is not
dangerous, but because they cannot properly regulate fear circuits, they
experience fear and anxiety in otherwise safe situations.