IONIC CONDUCTANCES CONTRIBUTING TO SPIKE REPOLARIZATION AND AFTER-POTENTIALS IN RAT MEDIAL VESTIBULAR NUCLEUS NEURONS

1. Intracellular recordings were made from 123 tonically active medial vestibular nucleus (MVN) neurones in a horizontal slice preparation o f the dorsal brainstem of the rat. On the basis of their averaged acti on potential shapes, the cells were classified as either type A, havin g a single deep after-hyperpolarization (AHP; 40/123 cells, 33%), or t ype B, having an early fast AHP and a delayed slow AHP (83/123 cells, 67%). The two cell types were distributed throughout the rostrocaudal extent of the MVN. 2. In type A cells TEA reduced the single deep AHP and decreased the rate of spike repolarization. Depolarizing current p ulses from a hyperpolarized membrane potential elicited spikes with sh ort plateau potentials in TEA. These persisted in Ca2+-free medium but were abolished along with the spontaneous activity in TTX. Ca2+-free medium did not affect the initial rate of repolarization but reduced t he deep AHP. Apamin and carbachol had little effect. 4-Aminopyridine ( 4-AP) slowed spike repolarization and the AHP amplitude by a small amo unt. Thus, in type A cells spike repolarization and AHP appear to be m ediated largely by a TEA-sensitive potassium current (presumably I-K) and an apamin-insensitive Ca2+-activated potassium current (presumably I-C). 3. The early fast AHP in type B cells was readily abolished in TEA. In seven of ten type B cells tested, the spontaneous spikes devel oped plateau potentials of 100-120 ms duration in 10 mM TEA, which the n became 7-9 s long in Ca2+-free medium. In the remaining three cells, the spontaneous plateaux were 1.75-2 s long in TEA, and were reduced to 30-100 ms in Ca2+-free medium. TTX abolished the spontaneous spikes and plateaux. The delayed AHP was abolished by apamin, which induced irregular firing. 4-AP slowed spike repolarization and abolished the f ast AHP, but did not induce plateaux. Thus, in type B cells spike repo larization involves a TEA-sensitive current (presumably I-K) as well a s I-O and the 4-AP-sensitive potassium current I-A, while the apamin I -AHP is responsible for the delayed AHP. 4. The tonic activity in type B cells appears to be regulated mainly by interactions between a pers istent Na+ current, which in most cells is large enough to generate pl ateaux when repolarization is impeded in TEA, and the hyperpolarizatio n mediated by I-AHP. About 30% of type B cells have an additional inwa rd Ca2+ current. In type A cells the persistent Na+ current is either not large enough to generate plateaus or is more effectively counterac ted by TEA-insensitive outward currents. The pacemaker conductances in type A and type B cells thus appear to be distinct.