Extensive experimental evidence suggests that carefully controlled spike times relative to theta-frequency network oscillations play an important role in hippocampal memory processing. Although excitatory phase response properties have been well characterized, how inhibitory inputs could control spike timing is less well studied. Here we report the control of spike timing during theta oscillation by inhibitory input and characterize the spike timing characteristics in spike time response curves (STRC). Using whole-cell patch-clamp recordings from CA1 pyramidal cells in vitro and with dynamic clamp to simulate theta-frequency oscillation (5 Hz), we show that GABA(A) receptor-mediated IPSPs can not only delay but also advance the postsynaptic spike time depending on the timing of the inhibitory input relative to the oscillation. The maximum spike time delay was 23.2 ± 2.9 ms and the maximum spike time advancement was -4.1 ± 1.4 ms (n = 5). Dynamic clamp-simulated artificial IPSP mimicking GABAergic input to the soma could also both delay and advance the spike time. The maximum spike time delay was 32.0 ± 2.1 ms and the maximum spike time advancement was -7.7 ± 0.8 ms (n = 8). The intrinsic mechanism underlying spike time advancement with IPSP is due to h-channels since the application of 10 μM ZD7288, an Ih channel blocker, completely abolished such advancement (n = 9). These results suggest that spike timing during theta-frequency oscillation can be bidirectionally controlled by inhibitory synaptic inputs and that the spike time advancement caused by IPSPs is due to h-channels intrinsic to the CA1 pyramidal neuronal membrane.