The striatum plays a vital role in coordinating motor planning, reinforcement, and motivation in the reward system. Striatal dopamine signaling and electrophysiological properties of medium spiny neurons in this region are sensitive to fluctuations in the sex steroid hormone 17β-estradiol (E2). Although previous work has focused on how ovarian or exogenous E2 influences the neurophysiology of reward-associated regions, striatal neurons also express aromatase, the enzyme responsible for catalyzing testosterone into E2. Currently, the role of aromatase and local E2 production in the striatum is not well understood, nor is its role in striatal neurophysiology. To address this question, we utilized a CRISPR/dCas9-based approach to upregulate expression of the aromatase gene (Cyp19a1) in rat primary striatal cultures. Neurons were transduced on DIV4 with CRISPR guide RNAs targeting either the Cyp19a1 gene or the bacterial control gene lacZ along with an enzymatically dead version of Cas9 (dCas9) tethered to a strong transcriptional activator, VPR (dCas9-VPR). After qPCR validation of aromatase up-regulation, we next asked whether this upregulation altered firing properties of striatal neurons by performing high-throughput electrophysiological recordings at DIV 11 using a multielectrode array (MEA) system. We found that upregulating aromatase expression in striatal neurons increased action potential frequency and total number of action potentials recorded. This indicates aromatase upregulation alters striatal physiology in vitro, possibly by increasing E2 production in striatal neurons. Future work will verify that Cyp19a1 upregulation increases E2 production, and determine whether estrogen receptor (ERα, ERβ, G-protein coupled ER) blockade suppresses observed increases in striatal neural activity.