Cdr1as is a circular RNA highly expressed in the brain, particularly in excitatory neurons. It is involved in a tightly regulated non-coding RNA network, interacting directly with miR-7. Recent studies have shown that, in mouse cortical neurons, Cdr1as buffers miR-7 activity to control glutamatergic transmission and neuronal network connectivity, which are crucial for long-lasting synaptic adaptations. Furthermore, Cdr1as expression was susceptible to external stressors, such as ischemia and sustained depolarization, subsequently affecting the regulation of glutamate release. These findings suggest that the circRNA might play a crucial role in activity-dependent gene regulation and activity-related disorders, such as epilepsy. Although this network is conserved among mammals, there has been no research into its function in human model systems. Therefore, our study aims to examine the network regulation in human iPSC-derived neurons and forebrain organoids. We generated human CDR1as knockout iPSC lines to investigate the consequences of perturbation of this regulatory network in human brain development and neuronal function. Using our model systems, we analysed the expression patterns of the network during organoid development using transcriptomics, and studied the effects on neuronal activity using electrophysiology. Additionally, we seek to understand the molecular mechanism through which the network controls glutamatergic release and comprehend the consequences of this regulatory network in seizure progression with an in vitro experimental epilepsy model.