The role of dopamine as a neurotransmitter in the human brain (2023)

VonOlivia Guy-Evans, released on February 22, 2022

vonSaul Mcleod, PhD

What is dopamine?

Dopamine is a neurotransmitter, a chemical messenger in the brain. Dopamine is an excitatory and inhibitory neurotransmitter and, as such, has a wide variety of effects on the brain, body and behavior.

It is known that dopamine is primarily associated with feelings of pleasure and reward. This chemical can also contribute to the following feelings:

  • monitoring

  • Focus

  • Motivation

  • kind

Dopamine is released when the brain expects a reward. The surge of dopamine in the brain when experiencing a pleasurable stimulus (eg, delicious food, video games, sex) can increase the desire to engage more with that stimulus because of the pleasurable sensation it evokes.

This is a cycle of motivation, reward and reinforcement. When you associate a certain activity with pleasure, sometimes even mere anticipation can be enough to spike your dopamine levels.

The right amount of dopamine is great for learning, planning, and productivity. For example, if someone has been working hard on a project for a long time, there may be a spike in dopamine activity after the project is completed.

The role of dopamine as a neurotransmitter in the human brain (1)

While heavily involved in pleasure and reward, dopamine is also involved in other functions:

  • motor functions

  • mood regulation

  • executive function

  • memory and concentration

  • Sleep

  • stress response

  • digestion and blood circulation.

It is important to note that dopamine does not act in isolation, but works together with other neurotransmitters and hormones such as serotonin and adrenaline to carry out a variety of functions.

Dopamine is a chemical belonging to the family of catecholamines and phenethylamines. Kathleen Montagu is believed to have first identified it in her 1957 paper, in which she demonstrated discoveries about important neurotransmitters.

As part of his research, he examined the levels of norepinephrine, epinephrine and 3-hydroxytriramine in tissues taken from the brain of different species.

Montagu speculated that there might be an additional catecholamine similar to hydroxytyramine, which he later confirmed was called dopamine.

Dopamine is highly concentrated in areas of the brain called the substantia nigra and the ventral tegmental area (VTA) in the midbrain. Other areas of the brain where dopamine can be produced are the hypothalamus and the olfactory bulb.

There are dopamine pathways that can be activated when exposed to a rewarding stimulus, resulting in more dopamine circulating to areas of the brain.

Role of dopamine in learning and motivation

reward system

Dopamine plays a key role in thisbrain reward system. This neurotransmitter helps reinforce certain behaviors that lead to reward.

In classic rat studies, a surge of dopamine causes the animal to repeatedly press a lever to obtain a food pellet.

This also works in humans, for example, when we decide to eat more of a pleasurable food, like another piece of cake, because we enjoy the satisfying feeling the food gave us.

reward prediction

Some studies have found that midbrain dopaminergic neurons can be activated by proximal contact (touching, tasting) with unexpected rewards.

As such events become predictable, neurons have been found to respond to more distal stimuli (visual or auditory) that precede and predict the availability of rewards.

The neurons would then stop responding to proximal contact with the reward (Romo & Schultz, 1990; Schultz et al., 1992).

This may be an oversimplification, as it has been found that neurons that no longer respond to proximal reward stimuli still respond to non-reward.

When the expected proximal contact does not occur, dopaminergic neurons are inhibited. Although dopamine release is triggered by the first reliable predictor of reward, midbrain dopamine is still sensitive to receipt or lack of reward.

The researchers examined the expectation of expecting a reward when gambling.

During the anticipation phase, when participants were told they could win money, blood flow was detected in the amygdala and frontal cortex, indicating activity in the brain.Nucleus accumbensand the hypothalamus, all rich in dopamine receptors.

The higher the potential reward, the more dopamine-driven brain activity was found.

reinforcement conditioning

By allowing dopamine to influence decisions, it can influence learned stimulus selection by the amount of positive or negative reinforcement the stimulus received.

The motivational cues associated with the reward can serve as conditioned reinforcers when given after a response.

For example, in a study with rats, they learned to work with thirst for the presentation of a light previously combined with water.

In this test, injections of amphetamine into the nucleus accumbens (a reward area of ​​the brain) causing dopamine release enhanced the light response (Taylor & Robbins, 1984), while selective dopamine lesions in the nucleus accumbens reduced this response (Taylor & Robbins, 1984). 1984). and Robbins, 1984). and Robbins, 1986).

Therefore, dopamine can modulate the expression of conditioned reinforcement, in addition to being essential for the establishment of conditioned reinforcers.

What does dopamine do in the brain?

The brain contains dopamine receptors, which are proteins found in the brain, neurons, and body. When a dopamine signal approaches a nearby neuron, it binds to that neuron's receptor.

The receptor and neurotransmitter work like a lock and key. Dopamine binds to the dopamine receptor and transmits its chemical message, causing changes in the neuron that received the signal.

Through the use of dopamine receptors, dopamine effects such as motor coordination, pleasure and cognition can be exerted.

Dopamine is produced primarily in an area of ​​the brain called the ventral tegmental area (VTA); a dopamine-rich nucleus in the midbrain.

Once produced in the VTA, dopamine is transported to other areas of the brain through various dopaminergic pathways, the two main pathways being mesolimbic and mesocorticol. Other pathways include the nigrostriatal and tuberoinfundibular pathways.

Dopamine pathways are neural connections where dopamine travels to areas of the brain and body to transmit important information, such as:

The role of dopamine as a neurotransmitter in the human brain (2)

mesolimbic pathways

This dopamine pathway is heavily involved in pleasure and reward functions. From the VTA, the dopamine produced here projects to the nucleus accumbens.

When present, dopamine primarily mediates feelings of pleasure and reward. For example, when someone eats a food they like, the VTA releases dopamine in the nucleus accumbens, creating positive feelings that reinforce the behavior.

Sometimes the stimuli can produce intense feelings of euphoria.

Located in the ventral striatum, the nucleus accumbens is part of a complex circuit involving the amygdala and hippocampus. Activation of the mesolimbic dopamine pathway signals that you want to repeat what just happened in order to feel the rewarding sensation again.

As the nucleus accumbens has connections with the amygdala, a region of the limbic system associated with emotions, this attributes feelings to the experienced reward.

Likewise, connections with the hippocampus, an area linked to memory, can attribute memories of pleasure to the experience to reinforce that feeling that is happening again.

Stimulating the nucleus accumbens is important for daily activities, but overstimulation can lead to craving the stimulus that stimulated it.


As with the mesolimbic pathways, the mesocorticol pathway begins with dopamine projections from the VTA. Signals are sent from the VTA to the prefrontal cortex, an area involved in cognition, working memory and decision making.

Therefore, activation of this pathway brings about the conscious experience of the pleasure and reward that is experienced. Attention, concentration and decisions can be made as a result of pleasure and reward.

Therefore, a dysfunction in this signaling pathway can lead to poor concentration and inability to make decisions.

vias nigroestriatais

This dopamine pathway is involved in movement planning. Dopamine projections begin in the substantia nigra, a basal ganglia structure located in the midbrain.

These projections go to the caudate and putamen, which are also part of the basal ganglia. Neurons in this pathway stimulate intentional movement and contain about 80% of the brain's dopamine.

When there is a reduction in the number of dopaminergic neurons in this pathway, it can lead to impaired motor control, including movement disorders such as Parkinson's disease.

Symptoms of dysfunction in this pathway can include spasms, convulsions, tremors and restlessness.

vias tuberoinfundibulares

The dopamine neurons in this pathway originate from the hypothalamus, an area that plays a role in hormone production and helps stimulate many important processes in the body.

Specifically, neurons are located in the arcuate and periventricular nuclei of the hypothalamus. These then project into the infundibular region of the hypothalamus. Thus, dopamine is released into the portal circulation that connects this region to the pituitary.

This is where dopamine acts to inhibit prolactin release. Prolactin is a protein secreted by the pituitary gland that enables milk production and plays an important role in metabolism, sexual satisfaction and the immune system.

Dopamine hypothesis in schizophrenia

The dopamine hypothesis for schizophrenia suggests that some of the symptoms of schizophrenia involve excessive dopamine activity.

Dopamine appears to play an important role in frontal and temporal lobe activity, particularly in parts of the brain.cerebral cortexthese lobes, which play a role in the cognitive, emotional, and perceptual functions that are often abnormal in schizophrenia.

There appear to be abnormalities in the mesocorticol and mesolimbic signaling pathways that transport dopamine from the VTA to areas of the cerebral cortex.

Changes in parts of the cerebral cortex are believed to cause many of the cognitive symptoms of schizophrenia, such as: B. disorganized thinking, difficulty integrating thoughts, and poor concentration.

Abnormal activity of dopamine pathways in the limbic system is believed to be responsible for many of the negative symptoms of schizophrenia, such as: B. Lack of motivation and social withdrawal.

Furthermore, it is believed that dopamine abnormalities in the temporal and prefrontal areas of the brain are overactive in people with schizophrenia and therefore can cause some of the positive symptoms of the disease, such as hallucinations and delusions.

This hypothesis makes sense because antipsychotic drugs that block the dopamine receptor in the brain appear to be effective in treating the positive symptoms of schizophrenia.

Likewise, with repeated exposure, the effects of dopamine-increasing drugs, such as methamphetamine and cocaine, can gradually induce paranoid psychosis in non-schizophrenic individuals.

This well-documented observation shows that sustained increases in dopamine activity can cause some of the similar symptoms of schizophrenia.

However, the dopamine hypothesis for schizophrenia may be an oversimplification, as there may be many more abnormalities in the neural network and neurotransmitter systems involved in causing the illness.

Research on the dopamine hypothesis has shown that disorders of glutamate, GABA, acetylcholine and serotonin are also involved in the pathology of schizophrenia, so it may not just be dopamine that affects this condition.

common questions

1. What happens when you run out of dopamine?

Low levels of dopamine can cause some of the following symptoms:

  • reduced attention

  • hard to focus

  • lack of motivation

  • poor coordination

  • movement difficulties

  • inability to feel pleasure.

In more extreme cases, a lack of dopamine can lead to conditions such as Parkinson's disease, dopamine transporter deficiency syndrome or depression.

While dopamine by itself cannot directly cause depression, it has been suggested that low levels of dopamine cause specific symptoms associated with the condition, such as problems with motivation, feelings of hopelessness and helplessness, and loss of interest in activities that were once enjoyed.

It is believed that these symptoms may be related to a dysfunction in the brain's dopamine system. A primary trigger for these disorders can be stress, pain, lack of sleep or trauma.

A physiological explanation is that there is decreased dopamine release from presynaptic neurons and/or impaired signaling, possibly due to changes in the number of dopamine receptors.

Attention Deficit Hyperactivity Disorder (ADHD) is a condition that is also associated with low levels of dopamine.

symptoms ofADHDThese include difficulty concentrating and paying attention, impulsiveness, and difficulty sitting still.

Because people with ADHD have low levels of dopamine, they are more likely to engage in behaviors to get more dopamine.

2. What are the symptoms of high dopamine?

High levels of dopamine can be euphoric in the short term, but harmful in the long term. In excess, dopamine can be a contributing factor to mania, hallucinations, and delusions.

Excess dopamine can lead to more competitive behavior, aggression, poor impulse control, gambling and addiction.

As such, addictive substances can raise dopamine levels and encourage the person to continue using these drugs to achieve that pleasurable feeling of reward.

This doesn't just have to be a drug addiction, people can become addicted to anything that gives them a dopamine boost, such as video games, food, and using social media.

3. How can I get my dopamine levels back to normal?

Depending on whether your dopamine levels are too high or too low will determine which techniques to use. If you want to increase dopamine levels, some ways can include:

  • Support a good sleep schedule

  • Less screen time (e.g. TV, phone), especially before bed

  • Learn to meditate or do mindfulness training

  • play sports regularly

  • Dietary changes to increase vitamin D and essential fatty acid levels

  • Physiotherapy for muscle pain and movement problems

  • Dopamine agonists: A class of drugs that bind to and activate dopamine receptors in the brain, mimicking the effects of natural dopamine in the brain.

For people with a lot of dopamine, such as B. people with schizophrenia, dopamine antagonists are usually recommended.

This is a class of drugs that bind to and block dopamine receptors, reducing dopamine activity.

Many antipsychotic medications are dopamine antagonists, such as chlorpromazine (Thorazine), risperidone (Risperdal), and clozapine (Clozaril).

4. What happens during a dopamine fast?

Dopamine fasting is a new trend in which people strive to "reset" their dopamine levels by completely abstaining from anything that gives them pleasure. This can include phone use, social media, video games, delicious food, sex, and social interaction.

Taking breaks from behaviors that trigger high levels of dopamine release can allow the brain to rest and recover, which is an antidote to the age of overstimulation we live in.

Kent Berridge, professor of psychology and neuroscience, suggests that taking a break from any (or all) stimulating activity won't reset your dopamine levels, but it might stop your dopamine system from firing all the time.

Dopamine fasting is not thought to lower dopamine, but taking breaks from one or two pleasurable activities at a time can help reduce impulsive behavior.

Additionally, one specific study showed that dopamine fasting from the social media platform Facebook for one week helped students regain 13.3 hours of their time and significantly reduced depressive symptoms by 17%, allowing them to engage in more behaviors. healthy (Mosquere et al., 2019).

About the author

Olivia Guy-Evans received her BA in Educational Psychology from Edge Hill University in 2015. She then received her Masters in Educational Psychology from the University of Bristol in 2019 for the past four years.

To reference this article:

Guy-Evans, O. (2022, February 22). The role of dopamine as a neurotransmitter in the human brain. Just Psychology.


Borenstein, J. (October 7, 2021). The role of dopamine in learning and memory. psychology today.

Brisch R, Saniotis A, Wolf R, Bielau H, Bernstein HG, Steiner J, Bogerts B, Braun K, Jankowski Z, Kumaratilake J, Henneberg, M. & Gos, T. (2014). The role of dopamine in schizophrenia from a neurobiological and evolutionary perspective: old fashioned but still fashionable. Frontiers in Psychiatry, 5, 47.

Bridges, N. (November 25, 2016). Dopamine pathways. Sanesco.

Conrad, B. (s.f.). The role of dopamine as a neurotransmitter in the human brain. enzo Retrieved November 5, 2021 from: brain/

Konkel, L. (August 10, 2018). What is dopamine? Daily Health.

Mosquera R, Odunowo M, McNamara T, Guo X and Petrie R (2020). The economic impact of Facebook. Experimental Economics, 23(2), 575-602.

Pietrangelo, A. (November 5, 2019). How does dopamine affect the body? health line.

Romo, R. and Schultz, W. (1990). Monkey midbrain dopamine neurons: contingencies of active touch responses during self-initiated arm movements. Journal of Neurophysiology, 63(3), 592-606.

Schultz W, Apicella P, Scarnati E & Ljungberg T (1992). Neural activity in the monkey ventral striatum associated with reward expectancy. Neuroscience Journal, 12(12), 4595-4610.

Sepah, C. (August 7, 2019). The Definitive Guide to Dopamine Fasting 2.0: The Hot Trend in Silicon Valley. LinkedIn.

Taylor, J.R. and Robbins, T.W. (1984). Behavioral control enhanced by conditioned reinforcers after microinjections of d-amphetamine into the nucleus accumbens. Psychopharmacology, 84(3), 405-412.

Taylor, J.R. and Robbins, T.W. (1986). 6-Hydroxydopamine lesions of the nucleus accumbens, but not the caudate nucleus, attenuate the heightened response to reward-related stimuli generated by intra-accumbens-d-amphetamine. Psychopharmacology, 90(3), 390-397.

Wise, R.A. (2004). Dopamine, learning and motivation. Nature Reviews Neuroscience, 5(6), 483-494.

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