Research explains why we get scared // Taking a peek behind fear

Movie audiences everywhere have been whipped into a state of highanxiety by Steven Spielberg's latest monster hit, "The Lost World."Today, scientists can reveal a profound new insight into what isgoing on in the brains of filmgoers as they wince, cringe and flinchat the antics of computer-generated dinosaurs.

The work of three Cambridge professors, Barry Everitt, TrevorRobbins and Simon Killcross, has cast new light on our most primitiveemotion - fear. Their work, published in the latest issue of thejournal Nature, provides insights that will aid the development ofdrugs to treat anxiety, and perhaps even addiction.

The prehistoric monsters in the film provide a good way toillustrate what is meant by fear. Their antics stimulate a defensesystem in the brain that first evolved to help animals cope withdanger, a mechanism that has been present since reptiles started towalk on Earth.

The Cambridge team has, for the first time, shown how twoquite distinct parts of this system form the seat of fear. Both areburied in a region found on either side of the brain called theamygdala, each the size and shape of an almond.

Three years ago, Anthony Damasio, a neurologist at theUniversity of Iowa, provided a stunning example of the importance ofthis brain structure through the study of "SM," a woman who suffereddamage to her amygdala.

SM failed what Damasio called the Doris Day test. "When weshowed her a film clip of Doris Day screaming, she asked, `What isshe doing?' " he said. As a result of her brain damage, SM isbaffled by manifestations of fear.

In "The Lost World," cast members are crunched like popcorn bymarauding dinosaurs. The Cambridge work shows that the reflex shockcreated by monster munches is controlled by only one part of theamygdala.

But the anxiety stimulated by the nerve-jangling score and theatmosphere of relentless threat, which is cultivated by sequencestaking place at night in the driving rain, affects a quite separatepart of the amygdala.

Traditionally, researchers have focused on one aspect of fear,the Pavlovian conditioned fear response that makes us startled ormakes us freeze.

Everitt gave one example of this response: "Imagine walkingdown a street in a foreign city, when someone runs up and mugs you.Next time you go to a city and you see someone running toward you,you will automatically feel those fear responses."

Thanks to the Cambridge work, we now know this response isgoverned by a structure at the heart of the amygdala, the centralnucleus, which is connected directly to the primitive centers in thebrain stem that regulate the outpouring of hormones, triggering aquickened heart rate, sweating, the freeze response or "jumping outof your skin."

But there is another dimension to fear, which comes fromanticipating a fright. It is the suspense that deters a formermugging victim from walking down a dingy alleyway.

The Cambridge discovery locates the anxiety response inanother nucleus of the amygdala, which can work separately from theone that makes us startled. This overturns the current picture ofhow the brain's fear center works.

Prevailing theory suggests that, to perceive a threat, ourexperience of the world must be associated with a memory of a fright.This requires the perception of the environment to be sent fromhigher centers of the brain, responsible for conscious thought, toeach amygdala, where a ripple of nerve activity passes from onenucleus to another.

But this notion of serial processing is not backed by theexperiments at Cambridge's department of experimental psychology.During a series of trials, rats could push one of two levers toobtain food. However, the food was accompanied by a light or a tone,and sometimes a mild "footshock."

The rats learned to associate the tone with the footshock.When confronted with the tone, the rats would freeze, if they had notavoided pressing the lever that produced the tone.

The team first showed that rats lacking the central nucleus ofthe amygdala never froze, but could be anxious enough to learn how toavoid the tone - the amygdala could still warn the higher braincenters.

When the rats lacked the outer, lateral, part of the amygdala,the Pavlovian response remained, but they were no longer able to takeavoiding action because they were unable to learn to associate thetone with the tingling (which then made them freeze). Therefore theinvoluntary, reflex fear responses are organized separately fromvoluntary fear avoidance within the amygdala.

Together, the nuclei of the amygdala provide both the fear ofcreeping along a dark corridor and the shock experienced when a doorthen bursts open. And it is because we possess this brain machinerythat Spielberg is able to scare us.

However, some people pay an unduly high price for their senseof fear. When overactive, this fear response is responsible forshyness, loss of self-confidence and disabling anxiety disorders.And here, says Everitt, the finding could have importantconsequences.

The current crop of drugs used to treat anxiety has beentested on the primitive fear response. Now it will be possible tofocus on how these drugs directly affect the avoidance response thatunderlies anxiety, offering the potential for more finely tunedtreatments.

There is another spin-off. The amygdala is also responsiblefor anticipating potentially pleasurable circumstances. "That ispretty important, since these stimuli are involved in cravings, forinstance for drugs or alcohol," said Everitt.