Computation in cortical networks depends on the balance between excitation and inhibition (Isaacson and Scanziani 2011, Neuron 72). Timed inhibition on specific somatodendritic domains of GABAergic neurons is needed to control the integration of their excitatory inputs and spike output. On the network level these functions support the generation of network oscillations and the recruitment of synchronously active principal cell assemblies (Klausberger et al. 2003, Nature 421). In the dentate gyrus, the primary input region of the hippocampus, a variety of inhibitory neurons are present which could participate in these tasks. These include perisoma-inhibiting interneurons (PIIs), proximal dendrite-inhibiting hilar commissural/associational pathway associated (HICAP) interneurons and distal dendrite-inhibiting hilar perforant pathway associated (HIPP) interneurons. Of these interneurons, the specific functions and contributions of the dendrite inhibiting interneurons (DIIs) still remain unclear. To address this question, we performed paired whole-cell recordings of synaptically connected DIIs in hippocampal slices to determine the functional and dynamic characteristics of synaptic GABA_A receptor-mediated signalling. Cells were labelled during recordings for subsequent morphological evaluation. Our data indicate that in contrast to strong, fast and reliable inhibitory signalling among PIIs (peak amplitude, 101 ± 35 pA; latency, 1.4 ±0.2 ms; failure rate, 2 ± 2 %; decay, 3.9 ± 0.8 ms), GABAergic transmission among mutually connected HICAP and HIPP cells is characterized by significantly weaker strength (HICAP pairs, 21 ± 11 pA; HIPP pairs, 7 ± 0.2 pA), higher failure rates (HICAP pairs, 58 ± 7 %; HIPP pairs, 45 ± 15 %) and markedly slower time courses (HICAP pairs, 7.2 ± 1.2 ms; HIPP pairs, 15.2 ± 1.8 ms) which may be explained by marked electrotonic attenuation and deceleration of synaptic signals (Nörenberg et al. 2010, PNAS 107). DIIs also demonstrate unique dynamic characteristics in their inhibitory signalling in response to 50 Hz trains. HICAP pairs show a continuous facilitation during the course of the train while HIPP pairs demonstrate an initial facilitation followed by depression. Coefficient of variance analysis indicates that both dynamic patterns are mediated by presynaptic mechanisms. Furthermore, DIIs also inhibit PIIs, such that the reliability and dynamics of inhibitory signalling are significantly affected by the identity of the presynaptic cell. In summary, our data show distinct kinetic and dynamic properties of compartment-specific dendritic inhibitory synapses. They further indicate a domain-specific inhibitory control of pathway-specific excitatory inputs onto target cells. Dendritic inhibition of interneurons could in effect ‘disinhibit’ the principal cell population specifically during activation by inputs from distinct extrahippocampal pathways. However, the precise roles of DIIs in controlling information processing will be the main focus of our future investigations.