A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.

Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. This process is called summation and occurs at the axon hillock. Whereas summation is temporal when the presynaptic neuron fires impulses in rapid succession. In a spatial summation, a postsynaptic neuron gets stimulated simultaneously by numerous presynaptic neurons.

Additionally, one neuron often has inputs from many presynaptic neurons, which can be excitatory or inhibitory—so IPSPs can cancel out EPSPs and vice versa. The net change in postsynaptic membrane voltage determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together, synaptic summation and the threshold for excitation act as a filter so that random "noise" in the system is not transmitted as important information.

The movement of three ions: sodium, potassium, and calcium, across the ion channels is responsible for voltage sensing, ion permeability, and the overall neuronal integration for the action potential propagation.

Sodium (Na⁺) Channels

Voltage-gated Na⁺ channels concentrated in the axon's initial segment and the Nodes of Ranvier allow the action potential initiation and propagation. These channels have an open, closed, and inactive conformation. In the closed and inactive states, the channel is impermeable to ion. This ion-impermeable state is essential for opening other channels that help in action potential propagation.

Potassium (K⁺) Channels

Numerous types of potassium channels are seen distributed in the soma, dendrites, juxtaparanodes, and nodes of the neuron that work to ensure the propagation of the impulse.

Delayed K⁺channels open only when the voltage-gated Na⁺ channels are not activated. Hence they are 'delayed' with respect to the Na⁺ current or Na⁺ ion flow, as these open slowly.

Rapid or fast inactivating K⁺-channels are inactive at resting membrane potential. When the membrane is sufficiently negative, these become available. In this way, they prolong the period between action potentials, thus maintaining the firing frequency.

A-type voltage-gated K⁺channels are rapidly inactivating channels that modulate the backpropagation of the action potential to the soma and dendrites. These channels help filter and shape electrical signals traveling between synapses and the soma and back from soma to synapses, preventing excessive firing.

Ca²⁺-activated K⁺channels are essentially potassium channels gated by voltage and raised calcium levels. The voltage-gated Ca²⁺ channels increase calcium levels and activate the K+ channels. The efflux of potassium ions makes membrane depolarization harder, allowing a delay between subsequent action potentials. Thus the neuron becomes less responsive to constant stimuli.

Calcium (Ca²⁺) Channels

Calcium channels are present on the axon terminals, soma, and dendrites. Voltage-gated Ca²⁺channels help release neurotransmitters from the presynaptic axon terminal. These also help in membrane depolarization by allowing calcium ion influx in the soma and dendrites.