Precisely controlled spike times relative to θ-frequency network oscillations play an important role in hippocampal memory processing. Here we study how inhibitory synaptic input during θ oscillation contributes to the control of spike timing. Using whole-cell patch-clamp recordings from CA1 pyramidal cells in vitro with dynamic clamp to simulate θ-frequency oscillation (5 Hz), we show that γ-aminobutyric acid-A (GABAA) receptor-mediated inhibitory postsynaptic potentials (IPSPs) can not only delay but also advance the postsynaptic spike depending on the timing of the inhibition relative to the oscillation. Spike time advancement with IPSP was abolished by the h-channel blocker ZD7288 (10 μM), suggesting that IPSPs can interact with intrinsic membrane conductances to yield bidirectional control of spike timing.
- CA1 pyramidal neuron
- Gamma-aminobutyric acid-A receptor
- Spike timing
- Theta oscillation
ASJC Scopus subject areas