Ionic conductances contributing to spike repolarization and after‐potentials in rat medial vestibular nucleus neurones.

Autor: Johnston, A R, MacLeod, N K, Dutia, M B
Zdroj: Journal of Physiology; November 1994, Vol. 481 Issue: 1 p61-77, 17p
Abstrakt: 1. Intracellular recordings were made from 123 tonically active medial vestibular nucleus (MVN) neurones in a horizontal slice preparation of the dorsal brainstem of the rat. On the basis of their averaged action potential shapes, the cells were classified as either type A, having a single deep after‐hyperpolarization (AHP; 40/123 cells, 33%), or type 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 pulses from a hyperpolarized membrane potential elicited spikes with short plateau potentials in TEA. These persisted in Ca(2+)‐free medium but were abolished along with the spontaneous activity in TTX. Ca(2+)‐free medium did not affect the initial rate of repolarization but reduced the deep AHP. Apamin and carbachol had little effect. 4‐Aminopyridine (4‐AP) slowed spike repolarization and the AHP amplitude by a small amount. Thus, in type A cells spike repolarization and AHP appear to be mediated largely by a TEA‐sensitive potassium current (presumably IK) and an apamin‐insensitive Ca(2+)‐activated potassium current (presumably IC). 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 developed plateau potentials of 100‐120 ms duration in 10 mM TEA, which then became 7‐9 s long in Ca(2+)‐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 Ca(2+)‐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 fast AHP, but did not induce plateaux. Thus, in type B cells spike repolarization involves a TEA‐sensitive current (presumably IK) as well as IC and the 4‐AP‐sensitive potassium current IA, while the apamin‐sensitive potassium current IAHP is responsible for the delayed AHP. 4. The tonic activity in type B cells appears to be regulated mainly by interactions between a persistent Na+ current, which in most cells is large enough to generate plateaux when repolarization is impeded in TEA, and the hyperpolarization mediated by IAHP. About 30% of type B cells have an additional inward Ca2+ current.(ABSTRACT TRUNCATED AT 400 WORDS)
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