Nonlinear synaptic integration in dendrites is a fundamental aspect of neural computation. One such key mechanism is the Ca2+ spike at the apical tuft of pyramidal neurons. Characterized by a plateau potential sustained for tens of milliseconds, the Ca2+ spike amplifies excitatory input, facilitates somatic action potentials (APs), and promotes synaptic plasticity. Despite its essential role, the mechanisms regulating it are largely unknown. Using a compartmental model of a layer 5 pyramidal cell (L5PC), we explored the plateau and termination phases of the Ca2+ spike under input current perturbations, long-step current-injections, and variations in the dendritic high-voltage-activated Ca2+ conductance (that occur during cholinergic modulation). We found that, surprisingly, timed excitatory input can shorten the Ca2+ spike duration while inhibitory input can either elongate or terminate it. A significant elongation also occurs when the high-voltage-activated Ca2+ channels (CaHVA) conductance is increased. ...