What you carry at this position in your DNA and what research says about it.
Dopamine Receptor Splicing: 5/10 evidence, 16 publications.
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Sample genotype (not yours): C/C
Typical Dopamine Splicing and Cognitive Efficiency
This genotype is associated with standard ratios of the short and long dopamine D2 receptor isoforms. It supports efficient prefrontal cortex activity during working memory tasks and typical susceptibility to substance abuse.
What this genotype means: Typical dopamine receptor splicing; Efficient prefrontal working memory processing; Better clinical response to rasagiline.
Sample genotype (not yours): A/A
Significantly Altered Dopamine Splicing and Highest Addiction Risk
Carrying two copies of the A allele causes the most pronounced shift in dopamine D2 receptor splicing. This genotype is linked to the lowest working memory efficiency and the highest risk of cocaine dependence.
What this genotype means: Lowest ratio of presynaptic D2S receptors; Substantially reduced working memory efficiency; Highest risk of cocaine dependence and toxicity.
Sample genotype (not yours): C/A
Altered Dopamine Splicing and Higher Addiction Risk
Carrying one copy of the A allele shifts the splicing of dopamine D2 receptors, reducing the presynaptic short form. This is linked to less efficient working memory processing and an increased risk of cocaine dependence.
What this genotype means: Reduced ratio of presynaptic D2S receptors; Less efficient prefrontal brain activation during memory tasks; Increased risk of cocaine dependence.
Gene function and biological role
Gene Function: The DRD2 gene encodes the dopamine D2 receptor, a key protein involved in the brain's reward, motor, and cognitive pathways. This receptor exists in two primary forms created by alternative splicing: a short isoform (D2S) that acts mainly presynaptically as an autoreceptor to regulate dopamine release, and a long isoform (D2L) that operates postsynaptically. Proper balance between these two isoforms is essential for maintaining healthy dopamine signaling in the striatum and prefrontal cortex. Alterations in DRD2 expression or splicing ratios are heavily implicated in neuropsychiatric conditions, including schizophrenia, substance abuse, and movement disorders.
Variant Impact: The rs2283265 variant is an intronic single-nucleotide polymorphism located in intron 5 of the DRD2 gene. Rather than altering the amino acid sequence of the receptor directly, this genetic change alters the mRNA splicing process. Specifically, the minor A allele decreases the expression of the short D2S isoform relative to the long D2L isoform. This shift in the D2S/D2L ratio alters dopamine autoreceptor function, leading to differences in prefrontal brain activity and cognitive performance.
Key Insight: The minor A allele of this variant changes how the brain splices the dopamine D2 receptor gene, reducing the short presynaptic version and forcing the prefrontal cortex to use more energy to perform working memory tasks.
Location: DRD2. Chromosome 11 · 11q23.2 · 113.4 Mb
Estimated prevalence by population
Global 70.5%; European 71.2%; African 83.0%; East Asian 34.1%; South Asian 54.1%; Americas 53.5%; Ashkenazi 79.7%; Finnish 62.1%; Middle Eastern 85.0%; Amish 81.6%.
Estimated CC genotype frequency.
Global 26.3%; European 26.4%; African 16.2%; East Asian 48.6%; South Asian 38.9%; Americas 39.3%; Ashkenazi 19.2%; Finnish 33.4%; Middle Eastern 14.4%; Amish 17.5%.
Estimated CA genotype frequency.
Global 3.2%; European 2.4%; African 0.8%; East Asian 17.3%; South Asian 7.0%; Americas 7.2%; Ashkenazi 1.2%; Finnish 4.5%; Middle Eastern 0.6%; Amish 0.9%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Neurology & Mental Health
Addiction & Reward
Cocaine Addiction Risk. Evidence: 5/10. Source: PMID 21150907. Typical Risk.
Memory, Learning & Attention
Working Memory. Evidence: 3/10. Source: PMID 18077373. Typical Efficiency.
Neurodegenerative Diseases
Rasagiline Response. Evidence: 5/10. Source: PMID 27190009. Stronger Response.
Neurodevelopmental Traits
ADHD Susceptibility. Evidence: 3/10. Source: PMID 24780147. Typical Risk.
Showing effects for A/A genotype
Cocaine Addiction Risk. Evidence: 5/10. Source: PMID 21150907. Highest Risk.
Working Memory. Evidence: 3/10. Source: PMID 18077373. Lowest Efficiency.
Rasagiline Response. Evidence: 5/10. Source: PMID 27190009. Typical Response.
ADHD Susceptibility. Evidence: 3/10. Source: PMID 24780147. Highest Risk.
Showing effects for C/A genotype
Cocaine Addiction Risk. Evidence: 5/10. Source: PMID 21150907. Increased Risk.
Working Memory. Evidence: 3/10. Source: PMID 18077373. Reduced Efficiency.
ADHD Susceptibility. Evidence: 3/10. Source: PMID 24780147. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having two copies of the C allele means your body produces typical levels of the presynaptic D2S autoreceptor relative to the postsynaptic D2L receptor. This balanced splicing ratio is associated with efficient brain activation patterns in the prefrontal cortex and striatum during working memory tasks. Studies suggest that individuals with this genotype do not carry the elevated risk of cocaine dependence or lethal cocaine toxicity associated with the minor A allele. Furthermore, in clinical studies of early Parkinson's disease, individuals with the C/C genotype demonstrated a significantly better response to the dopaminergic medication rasagiline compared to carriers of the A allele.
Typical dopamine receptor splicing; Efficient prefrontal working memory processing; Better clinical response to rasagiline.
Sample genotype: AA (Homozygous)
Having two copies of the minor A allele results in the most significant reduction in the expression of the presynaptic D2S receptor isoform. This substantial shift in alternative splicing impairs the brain's ability to regulate dopamine release via autoreceptors. Consequently, individuals with this genotype exhibit the least efficient prefrontal cortex activity during working memory tasks, requiring higher neural energy expenditures. Clinical studies have strongly linked this genotype to an increased risk of cocaine dependence and lethal cocaine toxicity. There is also an association with heightened susceptibility to ADHD and emotional dysregulation. Finally, individuals with this genotype do not experience the enhanced response to the Parkinson's drug rasagiline seen in C/C homozygotes.
Lowest ratio of presynaptic D2S receptors; Substantially reduced working memory efficiency; Highest risk of cocaine dependence and toxicity.
Sample genotype: CA (Heterozygous)
Carrying one copy of the minor A allele alters the splicing of the DRD2 gene, leading to a decreased ratio of the short D2S isoform relative to the long D2L isoform. Because the D2S isoform acts as a presynaptic autoreceptor regulating dopamine release, this shift can disrupt normal dopaminergic signaling. Neuroimaging studies show that carriers of this variant exhibit greater prefrontal cortex activation during working memory tasks, suggesting the brain must work harder to achieve the same cognitive performance. This genotype is also associated with an increased susceptibility to cocaine abuse and a higher risk of severe adverse outcomes from cocaine use. Additionally, carriers may show a more typical, less pronounced response to the Parkinson's medication rasagiline compared to those with the C/C genotype.
Reduced ratio of presynaptic D2S receptors; Less efficient prefrontal brain activation during memory tasks; Increased risk of cocaine dependence.
Variants with shared genetic architecture
rs2514218 · DRD2 Gene · Chr 11 · Mental Health Risk
rs1801028 · DRD2 Gene · Chr 11 · Schizophrenia Risk
rs6277 · DRD2 Gene · Chr 11 · Dopamine Receptor Function
Content updated August 2026.
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