Knowing Neurons
Brain Basics

Dopamine: More than just a pleasure molecule

By Keionna Newton

Dopamine. You’ve probably heard about it before in passing or perhaps you’ve seen it in the headlines. Perhaps you’ve seen people on social media using buzzwords like “dopamine hacking” or “dopamine detoxes”  and heard of promises about how to “optimize your dopamine.” In today’s world of endless information and distractions, dopamine seems to be one of social media’s favorite molecules to talk about, but what is dopamine really? Do any of these new promises about how to complete a “dopamine fast” for better health really warrant belief? Or are they just another social media fad? In short, dopamine is a neurotransmitter that is made in the brain to help coordinate processes such as learning, memory, movement, and attention. Exciting discoveries in neuroscience research have shown that dopamine is essential for a lot more than what was originally thought. Let’s take a deep dive and pit the facts against fiction about dopamine functions in the brain. 

Dopamine functions in the healthy brain:

Learning.  The most well-known function of dopamine in the brain is reward learning. During learning, dopamine has important roles in encoding valence, which can be thought of as the value of an event, object, or situation that can be positive or negative (Wert-Carvajal et al., 2022). Rather than signaling pleasure, the activity patterns of dopamine neurons are thought to be important for encoding the prediction of potential rewarding outcomes and associating these positive outcomes with their preceding cues (Glimcher, 2011). Numerous studies have shown that dopamine neurons increase their firing rates just before receiving a predicted reward (Schultz et al., 1997). This is true in the case of rats that are trained to press a lever in order to receive a pellet of food. Interestingly, these same dopamine neurons decrease their activity when the predicted rewarding outcome does not occur (i.e., a rat trained to press a lever does not receive the expected pellet of food) (Glimcher 2011). This concept is known as the reward prediction error, which is the difference between the expected reward and actual reward outcome. This phenomenon plays important roles in cognitive processes, such as reinforcement learning (Glimcher, 2011).

Memory. Dopamine-producing neurons reside in two regions deep in the brain, known as the ventral tegmental area (VTA) and substantia nigra pars compacta (SNpc) (Luo & Huang, 2016). Dopamine neurons send projections to other brain regions such as the striatum, the prefrontal cortex (PFC), and hippocampus, regions heavily involved in reward and memory formation (Luo & Huang, 2016; Sayegh et al., 2024; Clos et al.,2019; Axmacher et al., 2010; Jay, 2003). The subsequent release of dopamine is thought to alter synaptic plasticity (i.e., the change in strength of connections between neurons), aiding in the encoding and consolidation of memories, especially memories related to reward-cue associations (Bromberg-Martin et al., 2010; Dalley et al., 2005). Projections from the VTA are largely known for their roles in reward and goal-directed behaviors, while projections from the SNc are primarily known for their roles in voluntary movement (Morales & Margolis, 2017; Chinta & Andersen, 2005).

Motivation. The role for dopamine in regulating behaviors associated with motivation and reward-seeking is well-known. Dopamine is important for establishing a state of motivation which reinforces behaviors conducive to pursuing rewards in a goal-directed manner (Berridge & Robinson, 1998; Palmiter, 2008). For instance, one study conducted with genetically engineered mice that lacked sufficient dopamine levels in the striatum showed significant problems with motivated behaviors such as feeding (Palmiter, 2008). When dopamine levels in the striatum were restored in these mice with a drug known as L-DOPA (a precursor to dopamine that increases the availability of dopamine in the brain), these mice showed significant improvements in motivated behaviors related to feeding, movement, and reward-based learning.

Movement. The dopamine neurons that reside in the SNpc are part of a larger network of nuclei in a part of the brain known as the basal ganglia (Lanciego et al., 2012). The basal ganglia regulates brain functions such as movement as well as motor learning (learning associated with movement) and emotions (Lanciego et al., 2012). The release of dopamine at input nuclei in the basal ganglia is necessary for the proper control of movement, and dopamine dysfunction in the basal ganglia is associated with movement disorders such as Parkinson’s disease.

Cognition. As stated above, dopamine neurons deep in the brain send axonal projections to many brain regions, including the PFC. The PFC is important for cognitive control, which is the ability to act out behaviors that are in accordance with our goals. In addition, the PFC is also critical for executive functioning which enables effective planning, focusing attention, and remembering (Ott & Nieder, 2019). All of these cognitive processes require dopamine to work properly.

What happens when dopamine doesn’t function properly in the brain?

Aberrations in dopamine function are associated with several mood disorders, neurodevelopmental disorders, and neurodegenerative diseases. These conditions are very complex and there is still a lot of research that is needed in order to fully understand dopamine’s role in this vast array of conditions. However, many studies have revealed roles for dopamine dysfunction in conditions such as depression, bipolar disorder, schizophrenia, ADHD, Parkinson’s disease, and addiction (Mizuno et al., 2023; Ashok et al., 2017; Brisch et al., 2014; Tripp & Wickens, 2008; Ramesh & Arachchige, 2023; Wise & Robble, 2020).

What are the most common misconceptions about dopamine?

Dopamine is simply the “pleasure molecule.” This is one of the most popular misunderstandings surrounding dopamine function in the brain. Dopamine does contribute to your experience of pleasure (along with a host of other neurotransmitters), but experts now believe that dopamine has less to do with the actual creation of your experience of pleasure. More studies are showing that dopamine is better thought of as a chemical that allows us to predict rewarding and pleasurable outcomes and it increases our motivation to pursue rewards. In other words, dopamine is a chemical that helps link your behaviors with pleasurable experiences, reinforcing those behaviors and increasing your desire to want to do them again (Berridge, 2006).

You can “hack” “detox” or “fast” from dopamine. There is no scientific basis for the concepts of hacking, detoxing, or fasting from dopamine. You cannot detox your brain from dopamine, a neurochemical that supports many essential cognitive functions and whose release/action is not under your conscious control. When the media talks about “dopamine detoxes” or “dopamine hacking”, they are usually talking about ways to reduce your stress levels when it comes to overstimulating environmental factors like the information we are constantly being bombarded with on social media.

You can be addicted to dopamine. This is another popular myth about dopamine and is often brought up in the context of social media overconsumption during which people get a “dopamine hit” every time they check their Instagram for likes. While dopamine is likely involved in this behavior, you cannot be addicted to a neurochemical like dopamine, which is a biological necessity for proper communication between neurons. Dopamine is not innately good or bad, but is simply a neurotransmitter that is used as a signal for cell-to-cell communication in the brain. Even though dopamine itself is not addictive, dopamine does play a major role in addiction behaviors. Numerous studies have shown evidence for major changes in dopamine circuitry in the brain in people suffering from substance use disorders, and these findings have been modeled in animal studies as well (Volkow et al., 2009).

While the functions associated with dopamine mentioned above are by no means an exhaustive list, they are representative of the vast array of important brain processes that are mediated by this neurotransmitter. Reducing dopamine to a mere “pleasure molecule” misses the bigger picture. The brain is a complex organ, and almost nothing ever just impacts one neurotransmitter alone without impacting other neurochemicals in the brain. Similarly, dopamine in the brain is not inherently “good” or “bad.” For those looking for scientifically-backed ways to support their brain health throughout life, research shows that keeping to a regular sleeping routine, eating a healthy diet, and exercising regularly are the best ways to maintain brain health. No dopamine detox necessary.


Written by Keionna Newton
Illustrated by Kaitlyn Niznik
Edited by Liza Chartampila and Monserrat Orozco


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Ashok, A. H., Marques, T. R., Jauhar, S., Nour, M. M., Goodwin, G. M., Young, A. H., & Howes, O. D. (2017). The dopamine hypothesis of bipolar affective disorder: The state of the art and implications for treatment. Molecular Psychiatry22(5), 666–679. 

Axmacher, N., Cohen, M. X., Fell, J., Haupt, S., Dümpelmann, M., Elger, C. E., Schlaepfer, T. E., Lenartz, D., Sturm, V., & Ranganath, C. (2010). Intracranial EEG correlates of expectancy and memory formation in the human hippocampus and nucleus accumbens. Neuron65(4), 541–549. 

Berridge, K. C., & Robinson, T. E. (1998). What is the role of dopamine in reward: Hedonic impact, reward learning, or incentive salience? Brain Research Reviews28(3), 309–369. 

Berridge, K. C. (2006). The debate over dopamine’s role in reward: The case for incentive salience. Psychopharmacology, 191(3), 391–431.

Brisch, R., Saniotis, A., Wolf, R., Bielau, H., Bernstein, H. G., Steiner, J., Bogerts, B., Braun, A. K., Jankowski, Z., Kumaritilake, J., Henneberg, M., & Gos, T. (2014). The role of dopamine in schizophrenia from a neurobiological and evolutionary perspective: Old Fashioned, but still in Vogue. Frontiers in Psychiatry5

Bromberg-Martin, E. S., Matsumoto, M., & Hikosaka, O. (2010). Dopamine in motivational control: Rewarding, aversive, and alerting. Neuron68(5), 815–834. 

Chinta, S. J., & Andersen, J. K. (2005). Dopaminergic neurons. The International Journal of Biochemistry & Cell Biology, 37(5), 942–946. 

Clos, M., Bunzeck, N., & Sommer, T. (2019). Dopamine is a double-edged sword: Dopaminergic modulation enhances memory retrieval performance but impairs metacognition. Neuropsychopharmacology44(3), 555–563. 

Dalley, J.  W., Lääne, K., Theobald, D. E., Armstrong, H. C., Corlett, P. R., Chudasama, Y., & Robbins, T. W. (2005). Time-limited modulation of appetitive Pavlovian memory by D1 and NMDA receptors in the nucleus accumbens. Proceedings of the National Academy of Sciences102(17), 6189–6194. 

Glimcher, P. W. (2011). Understanding dopamine and reinforcement learning: The dopamine reward prediction error hypothesis. Proceedings of the National Academy of Sciences108(Suppl. 3), 15647–15654.

Jay, T. M. (2003). Dopamine: A potential substrate for synaptic plasticity and memory mechanisms. Progress in Neurobiology69(6), 375–390. 

Lanciego, J. L., Luquin, N., & Obeso, J. A. (2012). Functional neuroanatomy of the basal gangliaCold Spring Harbor Perspectives in Medicine2(12). 

Luo, S. X., & Huang, E. J. (2016). Dopaminergic neurons and brain reward pathways. The American Journal of Pathology186(3), 478–488. 

Mizuno, Y., Ashok, A. H., Bhat, B. B., Jauhar, S., & Howes, O. D. (2023). Dopamine in major depressive disorder: A systematic review and meta-analysis of in vivo imaging studies. Journal of Psychopharmacology37(11), 1058–1069. 

Morales, M., & Margolis, E. B. (2017). Ventral tegmental area: Cellular heterogeneity, connectivity and behavior. Nature Reviews Neuroscience, 18(2), 73–85. 

Ott, T., & Nieder, A. (2019). Dopamine and cognitive control in prefrontal cortex. Trends in Cognitive Sciences23(3), 213–234. 

Palmiter, R. D. (2008). dopamine signaling in the dorsal striatum is essential for motivated behaviors. Annals of the New York Academy of Sciences, 1129(1), 35–46. 

Ramesh, S., & Arachchige, A. S. (2023). Depletion of dopamine in Parkinson’s disease and relevant therapeutic options: A review of the literature. AIMS Neuroscience10(3), 200–231. 

Sayegh, F. J., Mouledous, L., Macri, C., Pi Macedo, J., Lejards, C., Rampon, C., Verret, L., & Dahan, L. (2024). Ventral tegmental area dopamine projections to the hippocampus trigger long-term potentiation and contextual learning. Nature Communications, 15(1). 

Schultz, W., Dayan, P., & Montague, P. R. (1997). A neural substrate of prediction and reward. Science, 275(5306), 1593–1599. 

Tripp, G., & Wickens, J. R. (2008). Research review: Dopamine transfer deficit: A neurobiological theory of altered reinforcement mechanisms in ADHD. Journal of Child Psychology and Psychiatry49(7), 691–704. 

Volkow, N. D., Fowler, J. S., Wang, G. J., Baler, R., & Telang, F. (2009). Imaging dopamine’s role in drug abuse and addiction. Neuropharmacology, 56, 3–8. 

Wert-Carvajal, C., Reneaux, M., Tchumatchenko, T., & Clopath, C. (2022). Dopamine and serotonin interplay for valence-based spatial learning. Cell Reports39(2), 110645. 

Wise, R. A., & Robble, M. A. (2020). Dopamine and addiction. Annual Review of Psychology71(1), 79–106. 


  • Keionna Newton

    Keionna is currently pursuing her PhD in Neuroscience in the lab of Dr. Lindsay De Biase at UCLA. She graduated from the University of Washington in 2021 where she used mouse models to investigate the cellular and molecular mechanisms of stress, pain, and addiction, with particular focus on kappa opioid receptors. Now at UCLA, Keionna’s research is focused on understanding how microglia modulate dopamine neuron circuitry in health and disease. Outside of the lab, Keionna enjoys hiking, backpacking, painting, reading books, and playing her guitar.

Keionna Newton

Keionna is currently pursuing her PhD in Neuroscience in the lab of Dr. Lindsay De Biase at UCLA. She graduated from the University of Washington in 2021 where she used mouse models to investigate the cellular and molecular mechanisms of stress, pain, and addiction, with particular focus on kappa opioid receptors. Now at UCLA, Keionna’s research is focused on understanding how microglia modulate dopamine neuron circuitry in health and disease. Outside of the lab, Keionna enjoys hiking, backpacking, painting, reading books, and playing her guitar.

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