In vitro characterization of neurons in the ventral part of the nucleus tractus solitarius. II. Ionic basis for repetitive firing patterns.

1. The ventral part of the nucleus tractus solitarius in guinea pigs comprises the dorsal respiratory group and is composed of three classes of neurons. These have been termed types I, II, and III. Each cell type possesses a unique set of repetitive firing properties. An in vitro brain stem slice preparation was used to study the ionic basis for these repetitive firing properties. 2. Three different membrane currents were shown to contribute to the repetitive firing properties. These were: a slow calcium current (ICa), an early, transient potassium current (IKA), and a calcium-activated potassium current (IKC). Type I and II neurons displayed physiologically significant amounts of these currents; type III neurons did not. 3. During depolarization from potential levels between -50 and -60 mV, the repetitive firing properties of type I and II neurons were determined primarily by ICa and IKC. IKA was inactivated in this potential range. The expression of IKC was greater in type I neurons than in type II neurons, and as a result, type I neurons exhibited a self-terminating burst of spike activity early in depolarization, whereas type II neurons displayed a gradual decline in spike frequency throughout depolarization. 4. The properties of IKA in type I and II neurons were studied using the single-electrode voltage-clamp technique. The kinetics of IKA in type I neurons was approximately twice as slow as those of type II neurons. In addition, the voltage dependence of activation and the removal of inactivation for IKA in type I neurons were shifted by about -10 mV with respect to type II neurons. 5. Depolarization of type I neurons from membrane potential levels where inactivation of IKA was removed caused a decrease in the frequency of the initial burst of spikes. This decrease in spike frequency was result of the coactivation of IKA with ICa. 6. Depolarization of type II neurons from membrane potentials where inactivation of IKA was removed caused a long delay between the onset of depolarization and the beginning of spike activity. The delay in excitation was modulated by both the magnitude and duration of the prestimulus hyperpolarization. This modulation of delayed excitation paralleled the time and voltage dependence for the removal of IKA inactivation in type II neurons.