It’s the little chill that goes through your body on dark nights. It’s the tingle at the back of your neck when you feel watched by hidden eyes. It’s the feeling that comes during a confrontation that lets you know somewhere in the distant past, your ancestors are raising their hackles and baring their teeth. The culprit, of course, is fear — a force as old as conscious life itself (or maybe even older).
Everyone knows what fear feels like, but what’s actually going on behind the scenes? What in our bodies and brains drives such a powerful and necessary emotion?
It’s a complicated journey, but the first step along the way is the amygdala. Dubbed “the brain’s computer processor of fear,” the amygdala receives visual, auditory and somatosensory input, and (through the hypothalamus) influences production of hormones like adrenaline. In addition, the amygdala can detect certain dangerous substances, such as carbon dioxide, and trigger an appropriate fear-based response.
Studies have shown that people with damaged amygdalas do not experience fear in the same way as most people. In the case of a woman with damage caused by Urbach-Wiethe disease, exposure to spiders, snakes and similar stimuli invoked only a rational response, not a physiological one. Even in personal situations that most people would find frightening, such as being held up at gunpoint, the woman reported that she did not feel fear.
The amygdala isn’t the only party responsible for this almost-universal experience, however. Certain genetic variations change how people experience fear, and how susceptible they are to it. Variations in the serotonin transporter gene and the gene for enzyme COMT can make people more susceptible to anxiety disorders, and cause a fearful response to a stimulus more quickly than in people without the variations. This research is an important indicator of interactions between environment and genetics, in which one’s genes can make one more or less susceptible to certain influences. Additionally, the environment influences (for better or worse) the way that certain genes are expressed.
Getting back to the brain, scientists have found that a growth factor in the prelimbic cortex is important in the formation of fear memories, and have identified neuronal circuits that control learning of fear and behavioral expression of fear. When researchers inactivated the lateral subdivision of the central nucleus of the amygdala in mice, the animals were unable to learn fear – in other words, to associate fear with a particular stimulus. When the medial subdivision of the same nucleus was inactivated, however, animals could learn fear, but could not act on it.
This information has the potential for very practical applications, such as helping scientists differentiate biologically between different kinds of fear and finding ways to treat fear-related disorders. While this kind of research is still in the works, and probably will be for quite a while, it may be comforting to note the hormone oxytocin – famous for stimulating intimacy and building trust – acts by suppressing the amygdala’s fear response. Until modern medicine finds a cure for the undercurrent of fear that has so far been a permanent part of the human condition, we can take comfort in activities such as cuddling — for science, of course.