Fear is a natural and primal emotion that has played an important role in the survival of humans and animals throughout evolution. The physical sensations of fear, such as increased heart rate, rapid breathing, and a surge of adrenaline, prepare the body for the common “fight-or-flight” response when faced with perceived danger. But what is happening on a neurological level when we experience fear? And does fear lead to an increase in the neurotransmitter dopamine? In this article, we will explore the complex relationship between fear and dopamine release in the brain.
What is dopamine?
Dopamine is one of the major neurotransmitters in the brain and plays a role in a variety of functions including motivation, pleasure, attention, learning, and movement control. Dopamine is produced in several areas of the brain, including the substantia nigra and ventral tegmental area, and it binds to dopamine receptors throughout the brain and body. When dopamine is released from neurons, it crosses synapses and binds to these receptors to transmit chemical signals between neurons.
Some key facts about dopamine:
- Dopamine is classified as a catecholamine neurotransmitter, along with norepinephrine and epinephrine.
- Low levels of dopamine are associated with conditions like Parkinson’s disease and depression.
- Many pleasurable activities like eating, sex, and exercise can trigger dopamine release.
- Addictive drugs like cocaine and methamphetamine affect dopamine signaling pathways, leading to euphoria and addiction.
- Dopamine plays a major role in the brain’s reward and pleasure centers.
Overall, dopamine helps regulate many important functions and plays a key role in motivation, learning, mood, movement, and how the brain perceives pleasure.
The fear response and dopamine release
When a threat or danger is detected, whether real or imagined, the body’s automatic fear response kicks in. The amygdala, the part of the brain that processes emotions like fear, triggers a cascade of neurological and physiological changes including:
- Increased heart rate and blood pressure
- Rapid breathing
- Sweating
- Muscle tension
- Heightened senses
- Increased alertness and focus
These reactions prepare the body to deal with threat through the fight-or-flight response. From an evolutionary standpoint, this fear response was essential for reacting quickly to danger and improving chances of survival.
During a fearful event, the amygdala communicates with other parts of the brain, including areas like the hypothalamus that control the pituitary gland and adrenal glands. This triggers the release of stress hormones including adrenaline (epinephrine) and cortisol. An influx of these hormones generates the physical sensations associated with fear.
But what about dopamine? Several studies have explored how fearful experiences impact dopamine signaling in animals and humans. The evidence suggests that dopamine release is Increased by some types of fearful stimuli, while other fear responses may actually decrease dopamine signaling.
For example, research has shown that rats demonstrate increased dopamine release in the prefrontal cortex region when exposed to a fearful event they cannot predict or control. The unpredictability seems to be an important factor.
In humans, one brain imaging study found increased dopamine release in the striatum area during anticipation of an unpredictable electrical shock. However, when the shocks were predictable, dopamine signaling decreased.
So in some cases, fear-inducing stimuli that are novel or unpredictable appear to trigger increased dopamine release. This may prime the brain to respond rapidly and learn from the new fearful situation.
The nuanced effects of fear on dopamine
However, more recent research suggests the relationship between fear and dopamine is complex and depends on the specific brain circuitry involved. Fearful events don’t always lead to increased dopamine activity.
For example, a neuroimaging study found decreased dopamine release in the prefrontal cortex when subjects were shown frightening video clips. This diminished dopamine response was associated with increased anxiety levels when subjects were under threat but could not take action.
Another animal study showed that rats demonstrating “freezing behavior” in response to a fearful stimulus had reduced dopamine release in the prefrontal cortex. Immobility is a passive fear response when fight-or-flight is not possible. In this case, this fearful behavioral response was associated with dopamine suppression, not release.
So in situations where fear triggers a passive or inhibited response, rather than an active one, dopamine signaling may become diminished. The behavioral response to fear seems to be an important factor.
Furthermore, the specific neural circuits involved play a role. One review noted that the amygdala, often considered the fear center of the brain, contains relatively few dopamine receptors compared to other regions. And dopamine neuron projections from the midbrain to the amygdala are scarcer than projections to other areas.
So the amygdala itself may not directly elicit dopamine release during fearful events. But dopamine changes can occur in other regions like the prefrontal cortex, nucleus accumbens, and hypothalamus that interact with the amygdala during fear.
In summary, research shows dopamine release is not a universal reaction to fear. The nuanced response depends on whether the fear prompts an active or passive reaction, as well as the specific neural circuits and brain regions involved.
The role of prediction in fear and dopamine
As mentioned earlier, predictability of a threat seems to play an important role in dopamine signaling changes. Unpredicted fearful stimuli often lead to dopamine increases, while predictable threats can result in dopamine suppression.
This effect is likely related to dopamine’s role in reinforcement learning and motivation. Dopamine neurons are activated when an unexpected reward occurs, or something is better than anticipated. This motivates us to repeat behaviors to obtain the reward again.
Conversely, dopamine decreases when something is worse than expected. This may reinforce avoidance of behaviors that fail to provide an expected positive outcome.
Similarly with fear, unpredictability signifies that the situation requires more learning and vigilance. Increased dopamine release may improve alertness and prime the brain to respond rapidly and learn from new threats in the environment.
In contrast, predictable negative outcomes like regular painful electric shocks lead to helplessness and suppressed dopamine activity. In unavoidable fearful situations, decreased dopamine may reflect despair and demotivation rather than an invigorated drive to act.
Effects of chronic stress and anxiety
While acute fearful events can cause complex changes in dopamine signaling, chronic fear, anxiety and stress also reshape dopamine pathways over time.
Prolonged stress and elevated cortisol levels can gradually suppress dopamine synthesis and release. Dopamine neurons have glucocorticoid receptors that bind cortisol, contributing to this effect.
Chronic stress may also decrease signaling through dopamine D2 receptors in the striatum area of the brain. Since D2 receptors inhibit dopamine release, lower D2 signaling can further disrupt optimal dopamine activity.
In addition, chronic anxiety and post-traumatic stress disorder (PTSD) have been associated with reduced density of dopamine transporters. Transporters recycle released dopamine, so fewer transporters may reflect lower overall dopamine function.
Through these various mechanisms, chronic fear, anxiety and trauma can significantly alter dopamine signaling, synthesis and receptor binding long-term. This may contribute to depression, lack of motivation and pleasure, and other mood changes often accompanying chronic stress.
Fear, dopamine and mental illness
Dysregulation of dopamine pathways is implicated in many mental health conditions beyond chronic stress. Imbalances in dopamine neurotransmission likely interact with fear and anxiety processing in complex ways to contribute to certain disorders.
For example, schizophrenia is associated with increased presynaptic dopamine activity, especially in the mesolimbic pathway that processes emotion and reward. Overactive dopamine function in these circuits may lead to mistaken or exaggerated fear reactions to neutral stimuli.
On the other hand, blunted motivation and difficulty experiencing pleasure in depression may be related to decreased dopamine neurotransmission, especially in the mesocortical pathway linking the midbrain and prefrontal cortex. This could impact cognitive processing of fearful stimuli and events.
Addictive drugs like cocaine or amphetamines can also profoundly alter dopamine signaling by blocking reuptake or stimulating release. With repeated use, dopamine pathways become dysregulated. This may decrease an individual’s ability to appropriately experience natural fear reactions that normally trigger avoidance of harmful substances or behaviors.
In patients with anxiety disorders like PTSD, some research points to altered dopamine signaling in regions like the insula and anterior cingulate cortex involved in processing emotional experiences. Irregularities in these dopamine pathways may be linked to exaggerated and uncontrolled fear responses.
Clearly, proper dopamine function plays an integral yet complex role in modulating emotions like fear within normal ranges. Further research on dopamine and fear pathways could aid development of improved treatments for mental illnesses like addiction, anxiety, depression and schizophrenia in the future.
Conclusion
In summary, acute fearful experiences can increase or decrease dopamine release depending on specific circuits activated and behavioral responses provoked. Unpredicted fearful stimuli tend to increase dopamine, while predictable threats can suppress dopamine activity instead.
Chronic stress and anxiety lead to gradual decreases in dopamine synthesis, release, signaling and receptor binding over time. Dysregulation of dopamine pathways likely contributes to abnormal fear and threat reactions in many mental health conditions.
The biochemistry of fear remains a very active area of neuroscience research. While dopamine is certainly involved, many neurotransmitters and brain structures interact during fear responses. Continued study of these complex pathways will further reveal the inner workings of emotions that are so vital for survival.
References
Study 1: Zack, M., Poulos, C.X., Fragopoulos, F., Woodford, T.M., & MacLeod, C.M. (2006). Negative affect words prime beer consumption in young drinkers. Addictive Behaviors, 31(1), 169-173. https://doi.org/10.1016/j.addbeh.2005.04.016
Study 2: Wassum, K.M., Ostlund, S.B., Loewinger, G.C., & Maidment, N.T. (2013). Phasic mesolimbic dopamine release tracks reward seeking during expression of Pavlovian-to-instrumental transfer. Biological Psychiatry, 73(8), 747-755. https://doi.org/10.1016/j.biopsych.2012.12.005
Study 3: Lammel, S., Lim, B.K., Ran, C., Huang, K.W., Betley, M.J., Tye, K.M., Deisseroth, K., & Malenka, R.C. (2012). Input-specific control of reward and aversion in the ventral tegmental area. Nature, 491(7423), 212-217. https://doi.org/10.1038/nature11527
Study 4: de Jong, J.W., Roelofs, T.J., Mol, F.M., Hillen, A.E., Meijboom, K.E., Luijendijk, M.C., van der Eerden, H.A., Garner, K.M., Vanderschuren, L.J., & Adan, R.A. (2015). Reducing Ventral Tegmental Dopamine D2 Receptor Expression Selectively Boosts Incentive Motivation. Neuropsychopharmacology, 40(9), 2085-2095. https://doi.org/10.1038/npp.2015.66
