The Neuroscience Behind Fear
What happens in our brain when we are afraid?
Our response to scary situations is often described as the “flight-or-fight” response. In a fear situation, our body produces adrenaline and groups of hormones called endorphins.
A 2008 study in the Journal of Neurology also found that flooding the brain with dopamine is also linked to behaviors suggestive of fear and paranoia in rats. Since dopamine is also associated with pleasure, its release in scary situations, along with a so-called “rush” of adrenaline and endorphins can lead to an elevated mood or high.
The “fear center” in the brain, is called amygdala. It’s placed between the temporal lobes, and is involved in how we process scary situations or threats. Animals with amygdala damage are observed to be tamer and have less of a flight-or-fight response.
Neural activity is also observed in the human amygdala, along with increased heart rate, when threats are introduced. Evidence for the dominant role in fear response played by the amygdala was further found in a 1995 study in the Journal of Neuroscience of a woman known as “SM” with a rare genetic disorder, Urbach-Wiethe disease, which caused her amygdala to harden and shrink. Not only could “SM” not recognize fearful expressions, she also showed no signs of it in typically scary situations like haunted houses or when surrounded by venomous snakes.
Innate or learned?
Some fears are innate, like the fear that tells you not to jump off that platform, even though you know you are safely tied to a bungee cord that will keep you from hitting the ground. We depend on these fears for our survival. However, we can also be conditioned to fear things that otherwise would not be scary.
Fear is an innate emotion that is triggered by environmental stimuli perceived as potentially threatening or harmful. Fear is an emotion whose existence is critical to survival.
Fear has long been thought to arise due to activity of cells in the amygdala, an almond-shaped brain structure located in the medial temporal lobe. In 1939, Heinrich Klüver and Paul Bucy reported that surgical removal of both temporal lobes (including the amygdalae) in monkeys produced a dramatic behavioral condition now referred to as the Klüver-Bucy syndrome. After surgery, the monkeys, who previously feared humans, no longer showed such fear.
They also showed a number of other behavioral changes, including hyperorality (a compulsion to examine objects by mouth), hypersexuality (excessive sexual behavior), hypermetamorphosis (excessive tendency to react to visual stimuli), and visual agnosia (inability to recognize familiar objects). The exact role of the amygdala in human fear, however, has not been fully established (perhaps) until now
Amygdala and fear-processing
Whether to Freeze, Flee, or Fight? It can make you run and hide, it can motivate you to take action, and it can freeze you dead in your tracks. In a 2010 study scientists in Italy at the European Molecular Biology Laboratory identified that a specific type of neurons in the amygdala determine how mice react to a frightening stimulus. Their findings revealed that deciding whether or not to freeze when you are faced with fear is a much more complex task for our brains than was formerly realized.
The scientists found that when they inhibited certain neurons in the amygdala of mice they were able to switch the response to fear from a passive stance to a more active one. Do human beings have the same response? Can we consciously condition ourselves to be more active and less passive in the face of fear?
I believe the answer is yes.”When we inhibited these neurons, I was not surprised to see that the mice stopped freezing because that is what the amygdala was thought to do. But we were very surprised when they did a lot of other things instead, like rearing and other risk-assessment behaviors,” says Cornelius Gross, who led the research at EMBL, “it seemed that we were not blocking the fear, but just changing their responses from a passive to an active coping strategy. That is not at all what this part of the amygdala was thought to do.”
Much to their surprise, the researchers found that the change from a passive to an active fear response was accompanied by the activation of large parts of the outer layer of the cerebrum called “the cortex.” Blocking this activation of the cortex could reinstate freezing behavior and flip the fear switch back to being passive.
A fast, subcortical pathway to the amygdala is thought to have evolved to enable rapid detection of threat. This pathway’s existence is fundamental for understanding nonconscious emotional responses, but has been challenged as a result of a lack of evidence for short-latency fear-related responses in primate amygdala, including humans.
Many experiments have been done to find out how the brain interprets stimuli and how animals develop fear responses. The emotion, fear, has been hard-wired into almost every individual, due to its vital role in the survival of the individual.
In fear conditioning, the main circuits that are involved are the sensory areas that process the conditioned and unconditioned stimuli, certain regions of the amygdala that undergo plasticity (or long-term potentiation) during learning, and the regions that bear an effect on the expression of specific conditioned responses.
These pathways converge in the lateral amygdala. Long-term potentiation (LTP) and synaptic plasticity that enhances the response of lateral amygdala neurons to the conditioned stimulus occurs in the lateral amygdala. As a result, the conditioned stimulus is then able to flow from the lateral amygdala to the central nucleus of the amygdala. The basal and intercalated masses of the amygdala connect the lateral amygdala with the central nucleus of the amygdala directly and indirectly. Pathways from central nucleus of the amygdala to downstream areas then control defensive behavior (freezing) and autonomic and endocrine responses.
What is the Difference Between Fear And Anxiety?
Let’s start with some definitions. What is fear? Fear is a feeling of disquiet that begins rapidly in the presence of danger and dissipates quickly once the threat is removed. It is generally adaptive.
Anxiety, on the other hand, is uneasiness over the anticipation of less specific or predictable threats. It lasts longer than fear and can also be adaptive.
When fear and anxiety are greater than expected or last beyond what is adaptive, affecting well being and function, then an anxiety disorder is present.
Fear can be innate or learned. Examples of innate fear include the fear of scorpions, snakes, or heights. Learned fear stimuli such as guns would not have been frightening to someone who lived in the 12th century, for example. Neither would images associated with man-made disasters or destruction such as a car accident or mushroom cloud.
Fear is highly preserved across animal species, so many species exhibit fear conditioning.
We now know from animal models of fear that the amygdala is central to the fear response. Sensory input reaches the sensory thalamus and then very quickly the amygdala which allows for a fear response, via the so called low road. This direct pathway to the amygdala is necessary but not sufficient, it cannot differentiate a snake from a stick.
The cortex is needed for conscious awareness, context, and perspective. That process is slower and occurs via the so called high road.
Here is a clinical example of how central the amygdala is to the fear response.
Patient SM has a very rare case of Urbach Wiethe disease, a congenital calcification of the amygdala bilaterally.
For many years, SM has repeatedly stated that she “hates” snakes and spiders. When asked to elaborate, SM reports that she simply does not like them and “tries to avoid them.” In order to assess the validity of SM’s claims, investigators took her to an exotic pet store that specializes in selling snakes and spiders.
Contrary to her verbally stated aversion to snakes and spiders, SM displayed a striking pattern of excessive approach-like behavior in concert with a lack of avoidance behavior; a pattern highly reminiscent of the behavior displayed by monkeys with focal amygdala lesions.
SM repeatedly approached all snakes, including holding and playing with a snake for over three minutes. She attempted to touch a tarantula, but had to be stopped due to the high risk of being bitten. She displayed a compulsive desire to want to “touch” and “poke” the store’s larger and more dangerous snakes, even though the store employee repeatedly told her that these snakes were not safe and could potentially bite.
When asked why she would want to touch something that she knows is dangerous and claims to hate, SM consistently replied that she was overcome with curiosity.
Throughout all of this SM’s reported experience of fear never surpassed a minimal level!
This shows the essential role of the amygdala in fear, a human emotion.
Animal models and safety learning are feasible and highly informative.
It is possible to have an objective measure of safety learning in animals and humans.
People with post-traumatic stress disorder do not respond appropriately to safety signals.
Understanding the neurobiology and safety circuits helps us to develop treatments for it and gives us more control over ourselves.
As always thanks for reading and until next time!