What we did:
This study highlights the relationship between receptor signaling, regional gene expression, and psychiatric disease mechanisms. These cross-species comparisons support the use of mouse dopamine receptor genes in modeling human disorders such as schizophrenia. In our research, we’ve found that altered D1 and D2 receptors are linked to symptoms of schizophrenia, where excessive striatal activity of these receptors can cause delusions, hallucinations, and executive function disorders.
How you can help:
One major knowledge gap we encountered was understanding how the DRD1 and DRD2 genes differentially contribute to schizophrenia compared to Parkinson’s disease. While the PubChem article linked both disorders to these dopamine receptors, it did not clearly explain what specific factors distinguish their roles in each disease. This raised questions about what mechanisms or regulatory differences lead to distinct neurological outcomes. Another gap involved dopamine expression in the brain, particularly why DRD1 and DRD2 receptors are highly expressed in the striatum compared to the prefrontal cortex. Further research into this could help clarify the functional role these receptors play in striatal signaling and behavior.
My favorite part of the project was exploring how a single set of genes can be involved in multiple neurological disorders, highlighting the complexity of brain chemistry and gene regulation. Investigating these overlaps made the project more engaging and emphasized the importance of deeper research to fully understand how dopamine receptors influence different disease processes.
I helped My group mates Harshpreet Kaur and Addisyn Braga research the mice genes Drd1 and Drd2 and how it correlated with Schizophrenia. Through our data portion we used the Anvil data base to come up with graph which showed how these two genes were greater expressed in the Striatum. Through different websites and articles I was able to formulate informations about not only the disease but also why these genes might show greater expression in the Striatum. My favorite part of this research assignment was learning the effects of Schizophrenia and just how similar the gene functions were between humans and mice. Putting all the information together my team and I organized our poster around our hypothesis. Some areas of research that could be deeper researched about would be what binds to these proteins to help them carry out their functions and could these binders further explain why the dopamine receptors were greatly expressed in the striatum in comparison to the prefrontal cortex. More information about drd1 and drd2 receptors in the Striatum can open up more correlations about the genes and why it’s present in that region of the brain. Lastly, also more research can be done between what happens or is taking place in the striatum with a human who has schizophrenia.
Contributing to the abstract and introduction for this poster gave me the opportunity to think deeply about how complex biological ideas are communicated to a broad scientific audience. Writing these sections required me to clearly frame the research question, explain the biological significance of dopamine receptor genes, and connect molecular-level mechanisms to real neurological conditions such as schizophrenia. This process helped me strengthen my understanding of how careful wording, structure, and context can shape how research is interpreted. It also reinforced the idea that strong scientific work is not only about data analysis, but about clearly explaining why the research matters. Overall, this experience increased my confidence in scientific writing and highlighted the importance of collaboration and clarity in communicating research findings.
