The hippocampus is essential for spatial navigation and memory processes. Hippocampal pyramidal cells (PCs) often exhibit complex spike bursts (CSBs) that are driven by regenerative dendritic Ca2+ plateau potentials. These events can induce rapid synaptic plasticity and new place field (PF) formation in CA1PCs. CA3PCs also fire CSBs, and their PF-inducing CSBs were shown to be particularly prolonged (Li et al, bioRxiv). However, the dendritic mechanisms underlying such long-lasting events in CA3PCs remain unclear. In acute rat brain slices, we observed large heterogeneity among CA3PCs in CSB prevalence and dendritic Ca2+ spikes kinetics, related to morpho-topographical properties of the cells. While many CA3PCs express long (~50 ms) compound Ca2+ spikes, some exhibit unusually short (few ms) Ca2+ spikes and no sustained CSB firing, raising the question whether specific conditions are required to facilitate prolonged plateaus in these cells. The neuromodulator acetylcholine (ACh) affects ion channels including those shaping Ca2+ spikes in CA3PCs, leading us to explore cholinergic regulation of Ca2+ spikes. The ACh receptor agonist carbachol (2 μM) robustly prolonged Ca2+ spikes, transforming short spikes into long-lasting forms and facilitating long-duration CSBs. In turn, blocking ACh receptors did not shorten Ca2+ spikes, suggesting that spike heterogeneity is not due to variable cholinergic tone in the slice. Optogenetic stimulation of cholinergic axons in transgenic mice increased CSB rate and duration. We propose that cholinergic neuromodulation can gate the ability of CA3PCs with short-duration Ca2+ spikes to generate sustained plateau potentials, providing a state-dependent dendritic mechanism for memory encoding and retrieval.