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Neuropathic pain is a chronic pain condition resulting from damaged peripheral nerves that induces allodynia (pathological touch sensitivity). Our previous studies suggest that prenatal alcohol exposure (PAE) is a risk factor for allodynia. In contrast to control rats, adult PAE rats with minimal nerve injury develop allodynia. Nerve-injured PAE rats display heightened peripheral and central nervous system (CNS) immune cell-derived proinflammatory cytokine production that consequently results in allodynia. This suggests that PAE dysregulates peripheral immune and CNS glial cell function to over-respond to subtle immune challenges leading to allodynia. However, gene expression profiles underlying dysregulated neuroimmune activity due to PAE are poorly understood. For the current study, the bioinformatics software, Ingenuity Pathway Analysis (IPA), was used to gain insight into key pathways and molecular targets underlying PAE’s effects on dysregulated neuroimmune function. Non-coding circular RNAs (circRNAs) are novel modulators of mRNA expression regulating CNS glial-immune function. Therefore, we hypothesized that circRNAs might be associated with critical neurological and immune dysfunction induced by PAE. Through IPA we identify the canonical pathways, diseases, and molecular functions, associated with the gene networks altered by PAE and nerve injury. Our microarray data identified 114 circRNAs that were differentially expressed in the spinal cord from PAE rats than in control rats following minor nerve injury, with ap value of< 0.05 and with a fold change> 1.5. Additionally, our data identified 15 circRNAs in blood …