Fast-spiking, parvalbumin-expressing basket cells (BCs) play a key role in feedforward and feedback inhibition in the hippocampus. However, the dendritic mechanisms underlying rapid interneuron recruitment have remained unclear. To quantitatively address this question, we developed detailed passive cable models of BCs in the dentate gyrus based on dual somatic or somatodendritic recordings and complete morphologic reconstructions. Both specific membrane capacitance and axial resistivity were comparable to those of pyramidal neurons, but the average somatodendritic specific membrane resistance (R m ) was substantially lower in BCs. Furthermore, R m was markedly nonuniform, being lowest in soma and proximal dendrites, intermediate in distal dendrites, and highest in the axon. Thus, the somatodendritic gradient of R m was the reverse of that in pyramidal neurons. Further computational analysis revealed that these unique cable properties accelerate the time course of synaptic potentials at the soma in response to fast inputs, while boosting the efficacy of slow distal inputs. These properties will facilitate both rapid phasic and efficient tonic activation of BCs in hippocampal microcircuits.cable models | dendrites | hippocampus | basket cell F ast-spiking, parvalbumin-expressing basket cells (BCs) play an important role in feedforward and feedback inhibition, providing rapid control over the frequency and timing of action potential initiation in principal neuron ensembles (1-6). Although inhibition comprises several steps, including activation of excitatory input synapses on BCs, dendritic integration of excitatory postsynaptic potentials (EPSPs), action potential initiation and propagation, and GABA release from output synapses, the kinetics of disynaptic inhibition can be very rapid, with ≈2 ms total onset time at physiologic temperature (3, 7). Several synaptic specializations contribute to the remarkable speed of feedforward and feedback inhibition. At the glutamatergic input synapses of BCs, the fast clearance of transmitter from the synaptic cleft and the expression of molecularly specialized L-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) contribute to rapid signaling (8, 9). At the GABAergic output synapses of BCs, the use of rapidly gated P/Qtype Ca 2+ channels and the tight coupling of these channels to the Ca 2+ sensors of exocytosis may serve a similar function (10, 11). Thus, functional specializations at both input and output synapses maximize the speed of BC-mediated disynaptic inhibition.Synaptic location, dendritic structure, and electrical cable properties will also contribute to rapid signaling in GABAergic interneurons. For example, the proximal location of excitatory synapses may promote rapid activation of BCs. The significance of this factor, however, is unclear, because many glutamatergic synapses terminate on distal dendrites of BCs (12). Furthermore, rapid signaling could be promoted by the extensive axon, which may accelerate the somatic EPSP decay time course by ge...

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