The hippocampal CA1 network supports gamma oscillations of variable frequencies, with fast (~80Hz) and slow (~40Hz) gamma occurring on different phases of the theta cycle (Colgin et al., 2009). It has been suggested that the fast and slow components are generated through distinct excitatory pathways, namely, perforant path and Schaffer collaterals respectively. However, the functional local circuitry that is recruited by the inputs to generate these gamma frequency bands remains to be determined. In order to investigate the local circuit mechanisms of oscillatory responses to variable excitatory drive, we induced oscillations in acute hippocampal slices in vitro. Mice (3 weeks) were transfected with the red-shifted depolarising opsin C1V1 (Yizhar et al., 2009) by stereotactic intrahippocampal injection (under isofluorane anaesthesia) of an adeno-associated virus with a Camk2α promoter. The virus was left to express for 4 weeks. Mice were sacrificed by transcardial perfusion with an N-Methyl-D-Glucamine based saline solution and acute horizontal slices prepared. We delivered variable intensity ramps of light to slices and simultaneously recorded the local field potential and whole-cell intracellular currents. Light ramps induced gamma frequency oscillations in the CA1 pyramidal cell layer (range=34 – 51 ±2 Hz, n=5. Means ± SEM. Recorded at 32οC). Phasic excitatory and inhibitory synaptic currents occurred in both principal cells and interneurons. Synaptic currents were superimposed on a direct C1V1-mediated current that was prominent in pyramidal neurons. Blocking glutamatergic synaptic transmission profoundly attenuated oscillations. Increasing the drive to the network increased oscillation frequency, and shifted the oscillation from an inhibition-dominant to an excitation-dominant regime. These findings suggest that differential recruitment of pyramidal cells and interneurons by CA1 afferents may contribute to the emergence of fast and slow gamma in vivo.