Who Needs Emotions? The Brain Meets the Robot

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then have a system that acts to reduce pain sensation? Endogenous opioids
appear to modulate pain responses, perhaps dampening the transmission in
pain fibers and pathways. One theory suggests that animals need to have a
pain-modulation system in the face of acute threat or danger, which is temporarily
activated but later deactivated when danger has subsided and recuperative
behaviors take over (Bolles & Fanselow, 1980; Fanselow & Sigmundi,
1986). Thus, if an animal is injured during attack or flight, activation of opioid
systems can reduce pain and facilitate adaptive escape. When the environment
becomes safe, recuperative behaviors, such as rest, “licking one’s
wounds,” and so on, are elicited. There is a large literature supporting the
contention that endogenous opioids are activated during situations of physical
or psychological stress (Bolles & Fanselow, 1982; Drolet et al., 2001). For
example, exposure of a rat to shock or a human to a painful stimulus raises
the pain threshold, but even exposure to non-physical stimuli such as conditioned
fear cues, novelty, or cat smell can provoke opioid-mediated analgesia
in rats (Bolles & Fanselow, 1982; Lester & Fanselow, 1985; Siegfried,
Netto, & Izquierdo, 1987). A further interesting example is that imminent
parturition in pregnant female rats results in a progressive opiate-mediated
analgesia, which subsides after birth; human birth is also associated with an
increase in circulating endorphins (Fajardo et al., 1994; Gintzler, 1980).
In addition to modulation of social bonding and pain, central opioids
appear to play a key role in the affective response to palatable food. Many
years ago, it was shown that morphine induces voracious eating in rats (Martin
et al., 1963). Since that time, there has been extensive research showing that
opioid activation of specific brain sites increases feeding, while antagonism
of central opiate receptors with drugs such as naltrexone reduces feeding
(reviews, Levine et al., 1985; Cooper & Kirkham, 1993; Kelley et al., 2002).
A major facet of current hypotheses concerning opioid modulation of food
intake is that opioids specifically regulate palatability and positive hedonic
evaluation of food. For example, in humans, experimental work shows that
naltrexone or naloxone reduces subjective ratings of food pleasantness while
leaving feelings of hunger and taste recognition unchanged and reduces preference
for sweet, high-fat foods (Fantino, Hosotte, & Apfelbaum 1986;
Drenowski et al., 1992). In the taste reactivity test, noted earlier, morphine
enhances taste palatability (Pecina & Berridge, 1995). In our own work in
rats, we have found that opioids, particularly those with a preference for
the mu receptor, potently increase the intake of normal chow as well as
sucrose, salt, saccharine, and fat when injected into the nucleus accumbens.
We have also found that rats thus treated will work harder and longer in
an operant task for sugar pellets, even when not food-restricted (Zhang,
Balmadrid, & Kelley, 2003). We have hypothesized that opioid-mediated
mechanisms in the nucleus accumbens (and undoubtedly other brain regions)