Dopamine is a powerful player in our cognitive function – impacting mood, movement, and motivation. Genetic variants in the dopamine receptors influence addiction, ADHD, neurological diseases, depression, psychosis, and aggression.
Please keep in mind as you read this article that I’m not a neuroscientist — instead, I’m just consolidating the research and translating it into something that is (hopefully) easier to read and apply. If you are under psychiatric care, do talk with your doctor before making any changes to anything you are currently doing.
What is dopamine?
Let’s start with the basics here. Dopamine acts as a neurotransmitter in the brain, transmitting a signal from one neuron to the next. It is a monoamine neurotransmitter, and also a catecholamine. A monoamine just means that it contains a single amine group – and this is important in the way that it is regulated in the brain.
Dopamine is derived from the amino acid tyrosine, which is converted to L-dopa and then to dopamine.
Dopamine is involved in:
- Sleep regulation
It acts on the dopamine receptors to cause motion and emotion.
Dopamine is important in how the brain controls movement, and it needs to be balanced. Too much dopamine leads to more movement – such as tics and involuntary movement. Too little dopamine leads to less movement – such as in Parkinson’s.
Dopamine is also important in emotions. Excess dopamine leads to euphoria, hallucinations, and psychosis. Dopamine causes conditioning – for example, learning either not to do something (via punishment) or learning to do something through reward. Not enough dopamine leads to anhedonia – that feeling of not caring about anything.
Dopamine also functions within the hypothalamus and pituitary gland to affect hormones. Specifically, dopamine inhibits prolactin. Without enough dopamine, it can lead to amenorrhea (lack of periods) in women and impotence and gynecomastia (moobs) in males.
Where is dopamine made?
There are two small regions deep in the brain where dopamine is made – the substantia nigra and the ventral tegmental area. From there, it travels via tracts to other areas of the brain.
What do the dopamine receptors do?
Dopamine doesn’t do anything by itself – it needs to bind with a receptor to cause an action. There are five different dopamine receptors in humans. They are coded for by the DRD1 through DRD5 genes. The receptors are responsible for the slightly different effects of dopamine in various brain regions.
The most common dopamine receptor in the brain is DRD1. It is found in several regions of the brain including the neostriatum, basolateral amygdala, cerebral cortex, hypothalamus, and thalamus.
The DRD1 receptor is linked to the effects of alcohol consumption. Blocking the DRD1 gene decreases the alcohol-seeking behavior in animal studies. It also decreases heroin and cocaine seeking-behavior.[ref]
Working memory – short-term memory needed for thinking and speaking – depends on the DRD1 receptors in the prefrontal cortex. Interestingly, working memory is considered to have a strong genetic component based on the DRD1 gene variants.[ref]
The DRD2 receptor is less abundant in the cerebral cortex than the DRD1 receptors, but it is abundant in other areas of the brain with dopaminergic neurons.
Both agonists and antagonists of the DRD2 receptor have been shown in animal studies to decrease alcohol and opiate consumption. The studies show that higher levels of either an agonist (something that stimulates the receptor) or antagonist (something that blocks the receptor) alter the addictive response.[ref]
The DRD3 receptor is found in the ventral striatum and other limbic areas. In humans, there are low amounts of the DRD3 receptors found in the cortical regions. This differs from other species and is a good reminder that animal studies may not be totally applicable to humans.[ref]
The DRD3 receptor has a higher affinity for dopamine (>20-fold higher than DRD2 receptors). This means that dopamine is more likely to bind with the DRD3 receptors, and high levels of dopamine will prompt the brain to make more DRD3 receptors. The ability to change with fluctuating dopamine levels makes the DRD3 receptor critical in dopamine-related functions and cognition.[ref]
This dopamine receptor is found at lower levels than DRD1 through DRD3. It is found in the retina, cerebral cortex, amygdala, hypothalamus, and pituitary. The DRD4 receptor hasn’t shown to be all that important in alcohol, opiate, or cocaine addiction.[ref]
The DRD5 receptor is very similar to the DRD1 receptor, and they are often located together. There seems to be a lot more research on DRD1, but often substances that bind to DRD1 also bind to DRD5.[ref]
How does dopamine relate to addiction?
Addiction to drugs causes compulsive drug-seeking behavior. The dopamine system is involved in the rewarding effects of drugs, and a lot of addictive drugs increase dopamine levels in certain regions of the brain. In fact, it has been known since the 1990s that blocking dopamine transmission takes away the reward effects of some addictive substances, such as cocaine and amphetamines.[ref]
There are three theories on how dopamine is related to addiction. First, the extra dopamine produced by addictive substances trains the brain through the reward system. It is the idea that the brain learns to like the drug, or makes it a habit. The second theory is that addictive substances change the brain circuits, making them hypersensitive. Third, researchers theorize that there is an imbalance between dopamine and other neurotransmitters. [ref]
Diseases associated with abnormal dopamine levels:
Several diseases are associated with altered dopamine.
- Parkinson’s disease – not enough dopamine due to degradation of the dopamine-producing area of the brain (substantia nigra)
- Tics / Tourettes – excess striatal dopamine due to GABAergic network dysfunction[ref]
- Psychosis – excess dopamine
- Schizophrenia – excess dopamine in some areas of the brain (causes hallucinations) and not enough in others[ref]
- Addiction – caused in part by repeated surges in dopamine (reward) and increased dopamine receptors
- ADHD -associated with low dopamine function in certain areas of the brain[ref]
- Bipolar affective disorder – high dopamine during mania which elevated DRD2 and DRD3 receptors, coupled with reduced dopamine during depression[ref]
- Anorexia – decreased reward (dopamine) for food along with other neurotransmitter imbalances[ref]
Dopamine receptor genetic variants:
Check your genetic data for rs4532 (23andMe v4, v5; AncestryDNA):
- C/C: increased risk of nicotine dependence[ref]; increased risk of treatment-resistant schizophrenia[ref]; better response accuracy in complex tasks[ref];
- C/T: increased risk of nicotine dependence[ref]; somewhat increased risk of treatment-resistant schizophrenia[ref]
- T/T: typical
Members: Your genotype for rs4532 is —.
Check your genetic data for rs5326 (23andMe v4, v5; AncestryDNA):
- T/T: decreased DRD1 in certain brain areas; increased risk of heroin addiction[ref]; poorer cognition and worse strategic planning[ref]
- C/T: increased risk of schizophrenia[ref] poorer cognition and worse strategic planning[ref]
- C/C: typical
Members: Your genotype for rs5326 is —.
Check your genetic data for rs686 (23andMe v4, v5; AncestryDNA):
- A/A: typical; more DRD1 expression
- A/G: intermediate DRD1 expression
- G/G: less DRD1 expression[ref]; decreased risk of rapid opioid dependence[ref]
Members: Your genotype for rs686 is —.
Check your genetic data for rs6277 (23andMe v4, v5; AncestryDNA):
- A/A: increased D2 receptor binding potential; increased susceptibility to stuttering[ref]; decreased risk of schizophrenia in Caucasians[ref]; better avoidance learning from negative outcomes[ref]; better rule-based learning[ref]
- A/G: common genotype in Caucasians
- G/G: typical worldwide; poorer performance on working memory test[ref]; decreased cognitive ability in older adults (compared to AA)[ref]
Members: Your genotype for rs6277 is —.
Check your genetic data for rs1801028* (23andMe v4; AncestryDNA):
- G/G: typical (Ser)
- C/G: may not respond as well to risperidone; increased risk of schizophrenia[ref]
- C/C: (Cys) may not respond as well to risperidone; increased risk of schizophrenia[ref]
*given in plus orientation to match 23andMe, AncestryDNA data
Members: Your genotype for rs1801028 is —.
The following variant is known as the DRD2 TaqI A variant, located in the ANKK1 gene. It is thought to be linked with a polymorphism in the DRD2 gene that affects its function.[ref]
Check your genetic data for rs1800497 (23andMe v4, v5; AncestryDNA):
- A/A: (DRD2*A1/A1) reduced number of dopamine binding sites[ref] increased risk of opioid dependence[ref]; increased BMI (susceptibility to food reward)[ref]; higher consumption of fried food[ref]; poorer working memory[ref]; increased suicide risk[ref]; increased risk of PTSD[ref] increased ADHD in males[ref]
- A/G: (DRD2*A1/A2) increased risk of opioid dependence; reduced number of dopamine binding sites; increased BMI (susceptibility to food reward)[ref]; higher consumption of fried food[ref] poorer working memory[ref]; increased risk of PTSD;
- G/G: (DRD2*A2/A2) typical; aerobic exercise increases motor learning[ref]
Members: Your genotype for rs1800497 is —.
Check your genetic data for rs6280 Ser9Gly (23andMe v4, v5; AncestryDNA):
- C/C: poorer executive function (psychosis patients)[ref], much better response to risperidone (antipsychotic used in autism)[ref]; increased risk of alcohol dependence[ref], decreased risk of bipolar disorder[ref]
- C/T: better response to risperidone (antipsychotic)
- T/T: typical
Members: Your genotype for rs6280 is —.
Check your genetic data for rs1800955 (23andMe v4 only):
- C/C: more likely to be a novelty seeker, more impulsive[ref]; more likely to smoke[ref]; more likely to take risks in ski/snowboarding[ref]; possibly less likely to become addicted to heroin[ref]
- C/T: somewhat more likely to be a novelty seeker; more likely to smoke
- T/T: typical
Members: Your genotype for rs1800955 is —.
The COMT gene codes for the enzyme that breaks down dopamine and other catecholamine neurotransmitters. A common variant can decrease or increase the speed at which this enzyme works.
- The G allele (Val) has higher COMT enzymatic activity, causing a more rapid breakdown of the neurotransmitters and thus lower levels of dopamine. In most populations, the G allele is the most common.[ref]
- The A allele (Met) has lower COMT enzyme activity and thus higher levels of dopamine. This variant of the COMT enzyme is said to have lower activity because it breaks down faster at normal body temperature.[ref]
Check your genetic data for rs4680 (23andMe v4, v5):
- G/G: higher COMT activity, lower dopamine & norepinephrine, higher pain tolerance (Val)
- A/G: intermediate COMT activity
- A/A: 40% lower COMT activity, higher dopamine & norepinephrine, lower pain tolerance (Met)
Members: Your genotype for rs4680 is —.
This gene codes for the dopamine transporter, known as DAT1. Below are just a couple of the variants in DAT1 — perhaps I’ll follow up with a longer article on this soon.
Check your genetic data for rs27072 (23andMe v4, v5):
- C/C: typical
- C/T: increased risk of bipolar disorder; increased risk of early smoking onset;
- T/T: increased risk of bipolar disorder[ref]; increased risk of early smoking onset[ref];
Members: Your genotype for rs27072 is —.
Again – let me caution that you don’t want to experiment with your neurotransmitters if you are under psychiatric care without talking with your doctor. Do more research, talk with your doctor/health care practitioner, and know what you are doing before you mess around here.
Diet – get enough protein to produce dopamine:
Dopamine is produced by converting the amino acid tyrosine first into l-dopa and then into dopamine. The body produces tyrosine from phenylalanine, which you get from your diet. You can also get tyrosine from foods. A diet that includes enough protein-rich foods (containing tyrosine/phenylalanine) is needed for dopamine production.[ref]
There have been several studies looking at the cognitive response in people who ate a diet lacking phenylalanine and tyrosine for a day. The results show that the acute decrease in dopamine changes response to timing, decreased functional connectivity in the brain, and slowed reaction time.[ref][ref][ref]
Natural dopamine receptor antagonists (blocks the receptor):
In general, atypical antipsychotic medications are antagonists of the DRD2 receptor. This makes sense when you think about too much dopamine causing hallucinations, euphoria, etc — things associated with a psychotic break.
Yohimbine is derived from the bark of an African tree, P. yohimbe, and traditionally used as an aphrodisiac (although human studies don’t really back that up). It is marketed as a supplement and used for weight loss. It acts on the adrenergic receptors, serotonin receptors, and is also an antagonist of the DRD2 and DRD3 receptors.[ref] Yohimbine is also used in animal studies to cause anxiety… so you may want to watch out for this as a side effect.[ref]
Ningdong granule is a traditional Chinese medicine preparation used for Tourette’s syndrome. It has been shown to regulate extracellular dopamine and also decrease binding to DRD2.[ref]
Natural ways to reduce dopamine:
An animal study showed that chronic lithium treatment – similar to prescription levels of lithium rather than supplemental lithium orotate – was able to blunt an anticipated spike in dopamine. This was thought to be one way that lithium may be effective in mania, which should be in a high dopamine state.[ref] Other studies, though, show that lithium increases dopamine following a TBI.[ref]
At least in rats, a ketogenic diet reduced the effects of daily cocaine injections.[ref] This is obviously not a study that is going to be repeated in humans…
In kids with epilepsy, when they went on a ketogenic diet to control the seizures, their dopamine metabolites decreased.[ref]
Natural dopamine receptor agonists:
L-theanine has been shown in animal studies to activate the DRD1/DRD5 receptors. Theanine is a component of green tea and is also sold as a supplement.
Natural dopamine boosters:
Sugar causes the release of dopamine. Research shows this is both from the taste of sugar and nutrition (energy) from sugar.[ref] You know how you read headlines stating that sugar is just like cocaine in the brain — well it turns out that isn’t really correct. Sugar affects dopamine in different areas of the brain (natural reward areas) than cocaine does.[ref]
Ginkgo biloba increases dopamine levels (in rat brains). The effect was seen after chronic (14-day) administration of the ginkgo.[ref][ref] Perhaps this is why Ginkgo Biloba is thought to increase memory…You can get ginkgo at your local health food stores or online.
Bacopa is an herbal supplement that is marketed as helping with brain function. In rats, bacopa decreased serotonin and increased dopamine. It has also been shown in studies to potentially help with dementia and Parkinson’s.[ref] You can get bacopa at health food stores or online.
Mucuna pruriens, aka velvet beans, have traditionally been cultivated as a vegetable in Asia, Africa, and the Pacific Islands. Mucuna prurien extract is high in l-dopa, the precursor to dopamine, and it has been used as a natural treatment for Parkinson’s.[ref] You can get a concentrated extract as a supplement — or perhaps you can find velvet beans at an ethnic grocery store in your area?
Related Genes and Topics:
Serotonin is a neurotransmitter that is important in depression, sleep, and many other aspects of health. Learn how your genetic variants in the serotonin receptor genes impact their function.
Wondering why your neurotransmitters are out of balance? It could be due to your COMT genetic variants. The COMT gene codes for the enzyme catechol-O-methyltransferase which breaks down (metabolizes) the neurotransmitters dopamine, epinephrine, and norepinephrine.
Baetu, Irina, et al. “Commonly-Occurring Polymorphisms in the COMT, DRD1 and DRD2 Genes Influence Different Aspects of Motor Sequence Learning in Humans.” Neurobiology of Learning and Memory, vol. 125, Nov. 2015, pp. 176–88. ScienceDirect, doi:10.1016/j.nlm.2015.09.009.
—. “Commonly-Occurring Polymorphisms in the COMT, DRD1 and DRD2 Genes Influence Different Aspects of Motor Sequence Learning in Humans.” Neurobiology of Learning and Memory, vol. 125, Nov. 2015, pp. 176–88. ScienceDirect, doi:10.1016/j.nlm.2015.09.009.
Balestri, Martina, et al. “Genetic Modulation of Personality Traits: A Systematic Review of the Literature.” International Clinical Psychopharmacology, vol. 29, no. 1, Jan. 2014, pp. 1–15. PubMed, doi:10.1097/YIC.0b013e328364590b.
Bolton, Jennifer L., et al. “Association between Polymorphisms of the Dopamine Receptor D2 and Catechol-o-Methyl Transferase Genes and Cognitive Function.” Behavior Genetics, vol. 40, no. 5, Sept. 2010, pp. 630–38. PubMed, doi:10.1007/s10519-010-9372-y.
Bombin, Igor, et al. “DRD3, but Not COMT or DRD2, Genotype Affects Executive Functions in Healthy and First-Episode Psychosis Adolescents.” American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics, vol. 147B, no. 6, Sept. 2008, pp. 873–79. PubMed, doi:10.1002/ajmg.b.30710.
Byrne, Kaileigh A., et al. “Dopaminergic Genetic Polymorphisms Predict Rule-Based Category Learning.” Journal of Cognitive Neuroscience, vol. 28, no. 7, July 2016, pp. 959–70. PubMed Central, doi:10.1162/jocn_a_00942.
Can, Adem, et al. “Chronic Lithium Treatment Rectifies Maladaptive Dopamine Release in the Nucleus Accumbens.” Journal of Neurochemistry, vol. 139, no. 4, Nov. 2016, pp. 576–85. PubMed Central, doi:10.1111/jnc.13769.
—. “Chronic Lithium Treatment Rectifies Maladaptive Dopamine Release in the Nucleus Accumbens.” Journal of Neurochemistry, vol. 139, no. 4, Nov. 2016, pp. 576–85. PubMed Central, doi:10.1111/jnc.13769.
Carlson, Shaun W., and C. Edward Dixon. “Lithium Improves Dopamine Neurotransmission and Increases Dopaminergic Protein Abundance in the Striatum after Traumatic Brain Injury.” Journal of Neurotrauma, vol. 35, no. 23, 01 2018, pp. 2827–36. PubMed, doi:10.1089/neu.2017.5509.
Chang, Yun-Hsuan, et al. “Genetic Variants of the BDNF and DRD3 Genes in Bipolar Disorder Comorbid with Anxiety Disorder.” Journal of Affective Disorders, vol. 151, no. 3, Dec. 2013, pp. 967–72. ScienceDirect, doi:10.1016/j.jad.2013.08.017.
Chen, Dingyan, et al. “Association between Polymorphisms of DRD2 and DRD4 and Opioid Dependence: Evidence from the Current Studies.” American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics, vol. 156B, no. 6, Sept. 2011, pp. 661–70. PubMed, doi:10.1002/ajmg.b.31208.
—. “Association between Polymorphisms of DRD2 and DRD4 and Opioid Dependence: Evidence from the Current Studies.” American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics, vol. 156B, no. 6, Sept. 2011, pp. 661–70. PubMed, doi:10.1002/ajmg.b.31208.
Chen, Jingshan, et al. “Functional Analysis of Genetic Variation in Catechol-O-Methyltransferase (COMT): Effects on MRNA, Protein, and Enzyme Activity in Postmortem Human Brain.” American Journal of Human Genetics, vol. 75, no. 5, Nov. 2004, pp. 807–21. PubMed, doi:10.1086/425589.
Coull, Jennifer T., et al. “Dopamine Precursor Depletion Impairs Timing in Healthy Volunteers by Attenuating Activity in Putamen and Supplementary Motor Area.” The Journal of Neuroscience, vol. 32, no. 47, Nov. 2012, pp. 16704–15. PubMed Central, doi:10.1523/JNEUROSCI.1258-12.2012.
Dahlin, Maria, et al. “CSF Levels of Dopamine and Serotonin, but Not Norepinephrine, Metabolites Are Influenced by the Ketogenic Diet in Children with Epilepsy.” Epilepsy Research, vol. 99, no. 1–2, Mar. 2012, pp. 132–38. PubMed, doi:10.1016/j.eplepsyres.2011.11.003.
Firouzabadi, Negar, et al. “DRD3 Ser9Gly Polymorphism and Its Influence on Risperidone Response in Autistic Children.” Journal of Pharmacy & Pharmaceutical Sciences: A Publication of the Canadian Society for Pharmaceutical Sciences, Societe Canadienne Des Sciences Pharmaceutiques, vol. 20, no. 1, 2017, pp. 445–52. PubMed, doi:10.18433/J3H63T.
Genis-Mendoza, Alma Delia, et al. “Association between Polymorphisms of the DRD2 and ANKK1 Genes and Suicide Attempt: A Preliminary Case-Control Study in a Mexican Population.” Neuropsychobiology, vol. 76, no. 4, 2017, pp. 193–98. PubMed, doi:10.1159/000490071.
He, Hairong, et al. “Associations between Dopamine D2 Receptor Gene Polymorphisms and Schizophrenia Risk: A PRISMA Compliant Meta-Analysis.” Neuropsychiatric Disease and Treatment, vol. 12, Dec. 2016, pp. 3129–44. PubMed Central, doi:10.2147/NDT.S118614.
—. “Associations between Dopamine D2 Receptor Gene Polymorphisms and Schizophrenia Risk: A PRISMA Compliant Meta-Analysis.” Neuropsychiatric Disease and Treatment, vol. 12, Dec. 2016, pp. 3129–44. PubMed Central, doi:10.2147/NDT.S118614.
Hildebrand, Patricia, et al. “Effects of Dietary Tryptophan and Phenylalanine-Tyrosine Depletion on Phasic Alertness in Healthy Adults – A Pilot Study.” Food & Nutrition Research, vol. 59, 2015, p. 26407. PubMed, doi:10.3402/fnr.v59.26407.
James, Morgan H., et al. “Cued Reinstatement of Cocaine but Not Sucrose Seeking Is Dependent on Dopamine Signaling in Prelimbic Cortex and Is Associated with Recruitment of Prelimbic Neurons That Project to Contralateral Nucleus Accumbens Core.” International Journal of Neuropsychopharmacology, vol. 21, no. 1, Nov. 2017, pp. 89–94. PubMed Central, doi:10.1093/ijnp/pyx107.
Kang, Seung-Gul, et al. “DRD3 Gene Rs6280 Polymorphism May Be Associated with Alcohol Dependence Overall and with Lesch Type I Alcohol Dependence in Koreans.” Neuropsychobiology, vol. 69, no. 3, 2014, pp. 140–46. PubMed, doi:10.1159/000358062.
Kehr, J., et al. “Ginkgo Biloba Leaf Extract (EGb 761®) and Its Specific Acylated Flavonol Constituents Increase Dopamine and Acetylcholine Levels in the Rat Medial Prefrontal Cortex: Possible Implications for the Cognitive Enhancing Properties of EGb 761®.” International Psychogeriatrics, vol. 24 Suppl 1, Aug. 2012, pp. S25-34. PubMed, doi:10.1017/S1041610212000567.
Le-Niculescu, H., et al. “Convergent Functional Genomics of Anxiety Disorders: Translational Identification of Genes, Biomarkers, Pathways and Mechanisms.” Translational Psychiatry, vol. 1, no. 5, May 2011, p. e9. PubMed Central, doi:10.1038/tp.2011.9.
Levran, Orna, et al. “Overlapping Dopaminergic Pathway Genetic Susceptibility for Heroin and Cocaine Addictions in African Americans.” Annals of Human Genetics, vol. 79, no. 3, May 2015, pp. 188–98. PubMed Central, doi:10.1111/ahg.12104.
Li, Lizhuo, et al. “The Association Between Genetic Variants in the Dopaminergic System and Posttraumatic Stress Disorder: A Meta-Analysis.” Medicine, vol. 95, no. 11, Mar. 2016, p. e3074. PubMed, doi:10.1097/MD.0000000000003074.
Ling, Daijun, et al. “Association between Polymorphism of the Dopamine Transporter Gene and Early Smoking Onset: An Interaction Risk on Nicotine Dependence.” Journal of Human Genetics, vol. 49, no. 1, 2004, pp. 35–39. PubMed, doi:10.1007/s10038-003-0104-5.
Mang, Cameron S., et al. “Exploring Genetic Influences Underlying Acute Aerobic Exercise Effects on Motor Learning.” Scientific Reports, vol. 7, no. 1, 21 2017, p. 12123. PubMed, doi:10.1038/s41598-017-12422-3.
Martinez, Luis A., et al. “A Ketogenic Diet Diminishes Behavioral Responses to Cocaine in Young Adult Male and Female Rats.” Neuropharmacology, vol. 149, 01 2019, pp. 27–34. PubMed, doi:10.1016/j.neuropharm.2019.02.001.
Mohammadi, Hiwa, et al. “Relationship between Serum Homovanillic Acid, DRD2 C957T (Rs6277), and HDAT A559V (Rs28364997) Polymorphisms and Developmental Stuttering.” Journal of Communication Disorders, vol. 76, Dec. 2018, pp. 37–46. PubMed, doi:10.1016/j.jcomdis.2018.08.003.
Naß, Janine, and Thomas Efferth. “Pharmacogenetics and Pharmacotherapy of Military Personnel Suffering from Post-Traumatic Stress Disorder.” Current Neuropharmacology, vol. 15, no. 6, Aug. 2017, pp. 831–60. PubMed Central, doi:10.2174/1570159X15666161111113514.
Nyman, Emma S., et al. “Sex-Specific Influence of DRD2 on ADHD-Type Temperament in a Large Population-Based Birth Cohort.” Psychiatric Genetics, vol. 22, no. 4, Aug. 2012, p. 197. journals.lww.com, doi:10.1097/YPG.0b013e32834c0cc8.
Nymberg, Charlotte, et al. “DRD2/ANKK1 Polymorphism Modulates the Effect of Ventral Striatal Activation on Working Memory Performance.” Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology, vol. 39, no. 10, Sept. 2014, pp. 2357–65. PubMed, doi:10.1038/npp.2014.83.
—. “DRD2/ANKK1 Polymorphism Modulates the Effect of Ventral Striatal Activation on Working Memory Performance.” Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology, vol. 39, no. 10, Sept. 2014, pp. 2357–65. PubMed, doi:10.1038/npp.2014.83.
Ota, Vanessa Kiyomi, et al. “DRD1 Rs4532 Polymorphism: A Potential Pharmacogenomic Marker for Treatment Response to Antipsychotic Drugs.” Schizophrenia Research, vol. 142, no. 1–3, Dec. 2012, pp. 206–08. PubMed, doi:10.1016/j.schres.2012.08.003.
Pan, Yuqing, et al. “Association of Dopamine D1 Receptor Gene Polymorphism with Schizophrenia: A Meta-Analysis.” Neuropsychiatric Disease and Treatment, vol. 10, June 2014, pp. 1133–39. PubMed Central, doi:10.2147/NDT.S63776.
Pinsonneault, Julia K., et al. “Dopamine Transporter Gene Variant Affecting Expression in Human Brain Is Associated with Bipolar Disorder.” Neuropsychopharmacology, vol. 36, no. 8, July 2011, pp. 1644–55. PubMed Central, doi:10.1038/npp.2011.45.
Rivera-Iñiguez, Ingrid, et al. “DRD2/ANKK1 TaqI A1 Polymorphism Associates with Overconsumption of Unhealthy Foods and Biochemical Abnormalities in a Mexican Population.” Eating and Weight Disorders: EWD, vol. 24, no. 5, Oct. 2019, pp. 835–44. PubMed, doi:10.1007/s40519-018-0596-9.
—. “DRD2/ANKK1 TaqI A1 Polymorphism Associates with Overconsumption of Unhealthy Foods and Biochemical Abnormalities in a Mexican Population.” Eating and Weight Disorders: EWD, vol. 24, no. 5, Oct. 2019, pp. 835–44. PubMed, doi:10.1007/s40519-018-0596-9.
Shafiei, Golia, et al. “Dopamine Signaling Modulates the Stability and Integration of Intrinsic Brain Networks.” Cerebral Cortex (New York, N.Y.: 1991), vol. 29, no. 1, 01 2019, pp. 397–409. PubMed, doi:10.1093/cercor/bhy264.
Shnitko, Tatiana A., et al. “Acute Phenylalanine/Tyrosine Depletion of Phasic Dopamine in the Rat Brain.” Psychopharmacology, vol. 233, no. 11, 2016, pp. 2045–54. PubMed, doi:10.1007/s00213-016-4259-0.
Sun, Xue, et al. “DRD2: Bridging the Genome and Ingestive Behavior.” Trends in Cognitive Sciences, vol. 21, no. 5, May 2017, pp. 372–84. PubMed Central, doi:10.1016/j.tics.2017.03.004.
—. “DRD2: Bridging the Genome and Ingestive Behavior.” Trends in Cognitive Sciences, vol. 21, no. 5, May 2017, pp. 372–84. PubMed Central, doi:10.1016/j.tics.2017.03.004.
Tellez, Luis A., et al. “Separate Circuitries Encode the Hedonic and Nutritional Values of Sugar.” Nature Neuroscience, vol. 19, no. 3, Mar. 2016, pp. 465–70. PubMed Central, doi:10.1038/nn.4224.
Tsang, Jonathan, et al. “The Relationship between Dopamine Receptor D1 and Cognitive Performance.” NPJ Schizophrenia, vol. 1, Mar. 2015, p. 14002. PubMed Central, doi:10.1038/npjschz.2014.2.
—. “The Relationship between Dopamine Receptor D1 and Cognitive Performance.” NPJ Schizophrenia, vol. 1, Mar. 2015, p. 14002. PubMed Central, doi:10.1038/npjschz.2014.2.
Vereczkei, Andrea, et al. “Multivariate Analysis of Dopaminergic Gene Variants as Risk Factors of Heroin Dependence.” PloS One, vol. 8, no. 6, 2013, p. e66592. PubMed, doi:10.1371/journal.pone.0066592.
Wang, Liang-Jen, et al. “A Potential Interaction between COMT and MTHFR Genetic Variants in Han Chinese Patients with Bipolar II Disorder.” Scientific Reports, vol. 5, Mar. 2015. PubMed Central, doi:10.1038/srep08813.
Xu, Haiyan, et al. “DRD2 C957T Polymorphism Interacts with the COMT Val158Met Polymorphism in Human Working Memory Ability.” Schizophrenia Research, vol. 90, no. 1–3, Feb. 2007, pp. 104–07. PubMed, doi:10.1016/j.schres.2006.10.001.
Yao, Jun, et al. “Association between DRD2 (Rs1799732 and Rs1801028) and ANKK1 (Rs1800497) Polymorphisms and Schizophrenia: A Meta-Analysis.” American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics, vol. 168B, no. 1, Jan. 2015, pp. 1–13. PubMed, doi:10.1002/ajmg.b.32281.
Yoshitake, T., et al. “The Ginkgo Biloba Extract EGb 761(R) and Its Main Constituent Flavonoids and Ginkgolides Increase Extracellular Dopamine Levels in the Rat Prefrontal Cortex.” British Journal of Pharmacology, vol. 159, no. 3, Feb. 2010, pp. 659–68. PubMed, doi:10.1111/j.1476-5381.2009.00580.x.
Zhu, Feng, et al. “Dopamine D1 Receptor Gene Variation Modulates Opioid Dependence Risk by Affecting Transition to Addiction.” PLoS ONE, edited by Huiping Zhang, vol. 8, no. 8, Aug. 2013, p. e70805. DOI.org (Crossref), doi:10.1371/journal.pone.0070805.