Modeling brain dynamics requires addressing processes that span different temporal and spatial scales [1]. This is crucial, when studying phenomena at the circuit level that are consequences of pharmacological or pathological alterations occurring at the single-cell level, such as changes in ionic or synaptic currents. Here, our aim is to study how single-cell dynamics interact with and affect circuit dynamics in a mouse model of autism (IB2 knock-out, KO), within the context of the cerebellar cortical microcircuit. In this work, we used a bottom-up approach: the microcircuit connectivity was reconstructed by placing all the cell types that characterize the cerebellar cortex, preserving their physiological morphology, density and connection affinity. On the simulation side, the activity of each cell type was reproduced through a multi-compartment model interfaced with the NEURON simulator [2]. The entire process was managed using the Brain Scaffold Builder tool [3,4]. The cerebellum’s implication in autism spectrum disorders (ASD) has been well-documented, with studies showing a dependent association between cerebellar damage and an increased risk for ASD [5]. We modified an existing wild-type granule cell (GrC) multi-compartment model [6] to replicate the empirical properties of the IB2-KO GrC as reported in [7]. This enabled us to construct the microcircuit of the granular layer by populating it with the IB2-KO GrC model, with the ultimate goal of extending it to include the molecular layer for a complete cerebellar cortex reconstruction. The IB2-KO GrC model exhibits higher maximum ionic conductances of Na and K compared to the physiological one. We adjusted the tonic glutamate level in the mossy fibers-GrC synaptic model and the NMDA maximum conductance to match experimentally observed I-f and NMDA current changes, predicting a baseline ambient glutamate level of ~28µM and an NMDA conductance change of ~7.5 times. Regarding the granular layer, we aim to replicate the spatially expanded higher E/I balance around the IB2-KO GrC observed in [7]. However, it is unclear if this phenomenon is solely due to the altered GrC or if Golgi cells are also involved. Our multiscale modeling approach can provide mechanistic insights into how effects at the circuit level emerge from alterations occurring at lower scales.