The integration of spatial information in the mammalian dentate gyrus (DG) is critical to navigation. Indeed, DG granule cells (DGCs) rely upon finely balanced inhibitory neurotransmission in order to respond appropriately to specific spatial inputs. This inhibition arises from a heterogeneous population of local GABAergic interneurons (INs) that activate both fast, ionotropic GABAA receptors (GABAAR) and slow, metabotropic GABAB receptors (GABABR), respectively. GABABRs in turn inhibit pre- and post-synaptic neuronal compartments via temporally long-lasting G-protein dependent mechanisms.The relative contribution of each IN subtype to network level GABABR signal setting remains unknown. However, within the DG, the somatostatin (SSt) expressing IN subtype is considered crucial in coordinating appropriate feedback inhibition on to DGCs. Therefore, we virally delivered channelrhodopsin-2 to the DG in order to obtain control of this specific SSt IN subpopulation in male and female adult mice.Using a combination of optogenetic activation and pharmacology, we show that SSt INs strongly recruit postsynaptic GABABRs to drive greater inhibition in DGCs than GABAARs at physiological membrane potentials. Furthermore, we show that in the adult mouse DG, postsynaptic GABABR signalling is predominantly regulated by neuronal GABA uptake, and less so by astrocytic mechanisms. Finally, we confirm that activation of SSt INs can also recruit presynaptic GABABRs, as has been shown in neocortical circuits. Together, these data reveal that GABABR signalling allows SSt INs to control DG activity and may constitute a key mechanism for gating spatial information flow within hippocampal circuits.Significance statement GABAergic interneurons provide powerful inhibition to cortical circuits, by directly regulating the activity of other neurons through metabotropic GABAB receptors. While much is known about the basic properties of GABAB receptor signalling, current knowledge of the relative contribution made by specific interneuron subpopulations to this inhibitory neurotransmission mechanism is less well understood. Our results help address this knowledge gap by showing that the somatostatin expressing interneuron subpopulation provide powerful GABAB receptor-mediated feedback inhibition in the mouse dentate gyrus. Furthermore, GABAB receptor activation in dentate gyrus was found to be tightly regulated by neuronal GABA uptake, and not astrocytes, thus providing self-regulated feedback inhibition. Together, these data provide novel insights into cell-type specific GABAB receptor-mediated control of dentate gyrus circuitry.