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The Neurobiology of Fear

Laurel Duphiney Edmundson

An animal's ability to experience fear is essential for its survival. Fear triggers the familiar "fight or flight" response, characterized by increased heart rate, breathing, and muscle tension, which allows the individual to escape from danger or defend itself against a predator. Based on the presence or absence of a stimulus, the brain appropriately regulates the strength and duration of this coping mechanism. When this regulatory system malfunctions, however, it can lead to excessive fearfulness in certain individuals. For some reason, these people have trouble suppressing the body's response to stress. While a lot of progress has been made in understanding the mechanisms that initially trigger fear responses, the precise method of turning them off remains elusive. Researchers continue to use animal models to gain further understanding into the regulation of the neurobiological reaction to fear.

The study of emotions as biological phenomena, which was once considered a "soft" subject area unworthy of serious inquiry, has garnered much interest and respect in the scientific community in recent years (3). Joseph Ledoux, a neuroscientist at New York University, is one of the pioneers in this area. In his research, he distinguishes between emotions and feelings, on the basis that "emotions are hard-wired, biological functions of the nervous system that evolved to help animals survive in hostile environments and procreate." Feelings, on the other hand, are "products of the conscious mind, labels (given) to unconscious emotions" and are therefore innately more difficult to understand (1). By viewing emotions as nervous impulses that elicit motor activity, instead of the complex workings of consciousness, Ledoux asserts that they can be studied quantitatively and understood more easily.

While not all scientists make this particular distinction between emotions and feelings, most would agree that the animal fear response involves more then just the physical preparation for "fight or flight." This initial, unspecific physiological response is followed by a slower, more detailed psychological assessment of the situation, during which the individual becomes conscious of feeling afraid. The walnut-sized structure in the forebrain called the amygdala, along with the hypothalamus, appear to control the first, physical response. When an animal receives a visual, auditory or other sensory stimulus that is recognized as potentially dangerous, the neurons from the eye or other sensory organ send a signal directly to the amygdala (2). The amygdala then stimulates the hypothalamus to produce corticotropin-releasing hormone (CRH). The release of CRH triggers the pituitary gland's discharge of adrenocorticotropic hormone (ACTH), which in turn stimulates the adrenal gland to secrete cortisol. Cortisol in the bloodstream causes an increase in glucose production, providing the necessary fuel for the brain and muscles to deal with stress (2).

Studies of neuronal activity in the brain have suggested that the prefrontal cortex, a cognitive and emotional learning center that helps interpret sensory stimuli, is responsible for the conscious assessment of danger. After passing through the amygdala, sensory information is sent on to the cortex. There, the frightening stimulus is examined in detail to determine whether or not a real threat exists. Based on this information, the amygdala will be signaled either to perpetuate the physical response or to abort it. Because the amygdala is aroused before the cortex can accurately assess the situation, an individual will experience the physical effects of fear even in the case of a false alarm (1).

Research conducted on rats has been useful in understanding the link between memory and emotions, including fear. The animal that has been conditioned by a paired tone (or flashing light) and a mild electrical shock, will exhibit fear whenever it is exposed to the same tone. The autonomic nervous system of the rat is activated as if it is faced with danger. Only after repeated presentations of the stimulus without the shock will the physical response diminish. Interestingly, evidence of continuing activity in the cortex has been found even after the physical response ceases. From this information, Ledoux and his colleagues have concluded that the memory of a traumatic experience can persist long after the event (5). This phenomenon explains why a human, who has been successfully treated for a certain phobia, still remembers that a certain stimulus used to cause him or her distress. Further studies performed by Ledoux et al. on rats revealed that damage to the prefrontal cortex made the suppression of fear difficult. This suggests that an excessively fearful individual might have a malfunctioning prefrontal cortex (5).

At the University of Wisconsin, Madison, Ned Kalin and Steven Shelton have focused their attention on the fear responses of rhesus monkeys to try to understand human models. They found a direct relationship between the amount of ACTH found in the blood of young monkeys and the duration and severity of their stress responses. (These stresses included separation from the mother and direct eye contact with a human observer.) Those individuals with lower baseline ACTH levels exhibited more moderate defensive behavior for a shorter duration than those with higher levels. A parallel phenomenon has been discovered in human children-those with lower basal cortisol levels also displayed less stress and inhibition. In another study, Kalin and Shelton discovered that youngsters in both groups developed behavioral patterns that resembled those of their parents; At five months of age, the monkeys' stress-induced ACTH level were similar to those of their mothers. Likewise, many of the extremely inhibited human children had overly anxious parents (6). From these results, Kalin and Shelton concluded that monkeys provide a good model for understanding some human behavior.

Based on colleague Richard Davidson's findings that the right prefrontal cortex is unusually active in extremely inhibited children, Kalin and Shelton began testing the effects of benzodiazepines on nervous activity. Administering these drugs to monkeys under stress significantly lessened electrical activity in the right prefrontal cortex. While this certainly seemed like it might be a successful therapy for extreme fearfulness, further testing had to be performed to insure their safety and effectiveness. Kalin and Shelton optimistically hypothesized that there might be a way to teach youngsters to regulate their benzodiazepine-sensitive systems without administration of medication (6).

The successes in animal research along with the power of computer-generated brain imaging has provided a solid understanding of the circuitry involved in generating the initial fear response in humans. However, researchers admit that "relatively little [is known] about the circuitry that's involved in turning it off." (2). Perhaps a better understanding of environmental and genetic factors that influence the development of the fear response will shed light on better ways to manage the expression of fear and its associated symptoms (2).

WWW Sources

1)New York Times online, limited archive access

2)The Scientist, Investigators pinpointing fear activity in the brain

3)News at University of Wisconsin, Madison, campus and community news

4)Stephen Maren, Ph.D. homepage, brief summary of research projects

5)APA Monitor, American Psychological Association publication

Other Sources "The Neurobiology of Fear." Ned H. Kalin, Scientific American, pages 94-101; May 1993.




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