The dentate gyrus (DG) of the hippocampus plays a key role in memory formation and associative binding in mammals. Neuromodulators are known to adapt circuit processing to enable plasticity, but the underlying mechanisms remain unclear. Previous work from our laboratory showed that endogenous acetylcholine (ACh) release enhances granule cell (GC) activity through a disinhibitory mechanism involving parvalbumin (PV) and somatostatin (SOM) interneurons. Here we developed a morphologically simple spiking network model (AdEx) of the DG, built upon prior DG models. The model includes GCs, mossy cells, PVs and SOMs, with the GC model extended to incorporate dendrites. Importantly, we distinguished two SOM subpopulations (HIPP and HIL) based on anatomical and physiological data. Model validation included intrinsic neuronal properties, firing rate–current curves, local field potential (LFP) spectra, and long-term potentiation simulations, consistent with published experiments. We then tested the hypothesis that strengthening SOM→PV connections mediates GC disinhibition. Simulations showed that enhancing HIL→PV synapses increased GC firing while reducing PV activity, whereas strengthening HIPP→PV connections failed to potentiate GCs within the tested range. Our results suggest that HIL interneurons are preferentially involved in cholinergic modulation of DG circuits, providing a mechanistic explanation for ACh-driven disinhibition and its role in learning-related plasticity.