By: Catherine Joachin

Dopamine

What is dopamine?

Dopamine is a monoamine neurotransmitter derived from the amino acid tyrosine (Cleveland Clinic, 2025). It serves as a chemical messenger between nerve cells and plays a crucial role in the reward system and regulating various bodily functions (Cleveland Clinic, 2025).

In the past, dopamine was associated with the ability to experience pleasure; however, recent studies show that increases in dopamine release are not unique to the presentation of a rewarding stimulus, suggesting a role related to motivation instead (Bressan & Crippa, 2005).

Dopamine Pathways and Their Functions

The substantia nigra, the ventral tegmental area, and the arcuate nucleus, located in the hypothalamus, are the brain’s main dopamine production sites (Olguín et al., 2015). Dopamine travels to different brain areas through several major circuits, including the mesolimbic pathway, which connects the ventral tegmental area to the nucleus accumbens (Olguín et al., 2015). Mesolimbic dopamine projects to limbic structures such as the hippocampus and the amygdala and regulates motivation, reinforcement, and reward-seeking behavior (Olguín et al., 2015).

Other important dopamine pathways include the nigrostriatal (or mesostriatal) pathway, which sends projections from the substantia nigra to the striatum, and the mesocortical pathway, which originates in the ventral tegmental area and stretches to the prefrontal cortex (Olguín et al., 2015; Baik, 2020). These pathways are responsible for motor control and cognitive functions such as attention and planning, respectively (Olguín et al., 2015; Baik, 2020). Recent data suggests that both nigrostriatal and mesolimbic dopamine projections also play a role in pain processing (Ziółkowska, 2021). Furthermore, dopamine is also involved in memory, mood regulation, sleep, arousal, learning, and lactation (Cleveland Clinic, 2025).

Dopamine-Related Complications

The depletion of dopaminergic neurons in the substantia nigra constitutes a hallmark of Parkinson’s disease that results in severe motor impairments, including tremors, rigidity, and slowness of movement (bradykinesia), as well as non-movement-related cognitive deficits (Ramesh & Molligoda Arachchige, 2023). Dopamine deficiencies are also associated with restless legs syndrome and attention deficit hyperactivity disorder (ADHD) (Cleveland Clinic, 2025). In contrast, high levels of dopamine are associated with mania, obesity, and addiction, the latter of which reflects an oversaturation of dopamine in brain structures associated with reward circuitry (Cleveland Clinic, 2025; Olguín et al., 2015).

Dopamine dysfunction is also linked to psychosis. The dopamine hypothesis of schizophrenia argues that changes in dopaminergic pathways contribute to positive (e.g., delusions and hallucinations) and negative symptoms (e.g., lack of motivation) of the condition (Cleveland Clinic, 2025; McCutcheon, Abi-Dargham & Howes, 2019).

Dopamine and Epilepsy

The role of dopamine in epilepsy has been scarcely explored; therefore, relevant literature on its involvement in the pathophysiology of seizures is fairly dated. Nevertheless, studies have shown that dopamine may be involved in processes associated with temporal lobe epilepsy as well as comorbid anxiety and depression through changes in D1 and D2 receptor signaling, suggesting that dopamine plays a significant role in modulating seizure activity through the limbic system (Rocha et al., 2012; Bozzi & Borrelli, 2013).

Conclusion

Dopamine is a chemical that modulates the brain’s reward system and other important bodily functions. It activates several brain structures through a series of pathways connecting important dopamine-production sites to areas responsible for attention, learning, memory, and movement. While its involvement in seizure development is not extensively studied, it is suggested that alterations to dopamine receptor subtypes and region-specific brain activation play a role in epilepsy.

References

Baik, J.-H. (2020). Stress and the dopaminergic reward system. Experimental & Molecular Medicine, 52(12), 1879–1890. https://doi.org/10.1038/s12276-020-00532-4

Bozzi, Y., & Borrelli, E. (2013). The role of dopamine signaling in epileptogenesis. Frontiers in Cellular Neuroscience, 7, 157–157. https://doi.org/10.3389/fncel.2013.00157

Bressan, R. A., & Crippa, J. A. (2005). The role of dopamine in reward and pleasure behavior – review of data from preclinical research. Acta Psychiatrica Scandinavica, 111(s427), 14–21. https://doi.org/10.1111/j.1600-0447.2005.00540.x

Cleveland Clinic. (2025). Dopamine. Cleveland Clinic. https://my.clevelandclinic.org/health/articles/22581-dopamine

McCutcheon, R. A., Abi-Dargham, A., & Howes, O. D. (2019). Schizophrenia, Dopamine and the Striatum: From Biology to Symptoms. Trends in Neurosciences (Regular Ed.), 42(3), 205–220. https://doi.org/10.1016/j.tins.2018.12.004

Olguin, H. J., Guzman, D. C., Garcia, E. H., Mejia, G. B., & Bulteau, A.-L. (2016). The Role of Dopamine and Its Dysfunction as a Consequence of Oxidative Stress. Oxidative Medicine and Cellular Longevity, 2016(2016), 1–13. https://doi.org/10.1155/2016/9730467

Ramesh, S., & Arachchige, A. S. P. M. (2023). Depletion of dopamine in Parkinson’s disease and relevant therapeutic options: A review of the literature. AIMS Neuroscience, 10(3), 200–231. https://doi.org/10.3934/Neuroscience.2023017

Rocha, L., Alonso-Vanegas, M., Villeda-Hernández, J., Mújica, M., Cisneros-Franco, J. M., López-Gómez, M., Zavala-Tecuapetla, C., Frías-Soria, C. L., Segovia-Vila, J., & Borsodi, A. (2012). Dopamine abnormalities in the neocortex of patients with temporal lobe epilepsy. Neurobiology of Disease, 45(1), 499–507. https://doi.org/10.1016/j.nbd.2011.09.006

Ziółkowska, B. (2021). The Role of Mesostriatal Dopamine System and Corticostriatal Glutamatergic Transmission in Chronic Pain. Brain Sciences, 11(10), 1311-. https://doi.org/10.3390/brainsci11101311