There are several inward currents that help produce action potentials and bursts in pacemaker neurons. There are two main voltage dependent sodium currents that contribute to the depolarization and firing of action potentials in neurons. The fast and transient sodium current produces a large depolarization that fires the initial action potential in neurons, however this current is quickly inactivated and does not help maintain bursting activity in neurons. To achieve bursts, a persistent sodium current provides enough depolarization to facilitate the firing of action potentials during a burst. Unlike the fast and transient sodium current, the persistent sodium current (INaP) is activated at very low membrane potentials and has a much slower inactivation, which allows neurons to intrinsically fire action potentials at sub-threshold membrane potentials. Studies have shown that the inactivation of this persistent sodium current helps end bursts in pacemaker neurons. The amount of time it takes for INaP to become activated again establishes the timeframe between each burst. The neuron can receive synaptic inputs and different amounts of inward and outward currents to regulate the time between each burst, which ultimately helps generate a specific breathing pattern.