Stimulation of the fimbria in rat hippocampal slices evoked an extracellular negativity in the granule cell layer and a small depolarization in granule cells at their resting potentials. The intracellular potentials appeared to be GABA A receptor-mediated IPSPs because they reversed at −69.1 ± 1.0 mV (mean ± S.E.M., n = 14) and were blocked by the GABA A receptor antagonist bicuculline (10–50 μM, n = 14). However, during the first few minutes of perfusion with bicuculline, IPSPs transiently and paradoxically increased in amplitude. As IPSPs increased, the reversal potential and latency to onset remained the same. These effects were reversible, and during the wash period IPSPs first increased and then stabilized at a smaller amplitude, similar to IPSPs evoked in control conditions. As the GABA A receptor-mediated IPSP decreased, it was followed by a second hyperpolarization. This late hyperpolarization appeared to be a GABA B receptor-mediated IPSP, because it reversed near the equilibrium potential for potassium (mean −81.8 ± 2.3 mV, n = 12, [K +] o = 5 mM) and was blocked by the GABA B receptor antagonist 2-hydroxy saclofen (250–500 μM, n = 5). The results suggest that GABA A and GABA B receptor-mediated IPSPs evoked in granule cells by fimbria stimulation are normally inhibited by activation of GABA A receptors. The inhibition by GABA A receptors is strong enough that, in control conditions, the GABA A IPSPs are barely detectable and the GABA B IPSPs are undetectable. The relevant GABA A receptors could be located presynaptically, on the nerve terminals of inhibitory interneurons that innervate granule cells, or on the dendrites and somata of the interneurons, where they may be affected by GABAergic inputs activated by fimbria stimulation. These data demonstrate the strength and complexity of pathways utilizing GABA A receptors and GABA B receptors to inhibit dentate granule cells.