Abstract

Medial vestibular nucleus (MVN) neurons are found to have spontaneous electrical activity in the absence of any detectable synaptic input. To investigate the contributions of intrinsic mechanisms to the spontaneous activity of type B MVN neurons, we examined the effects of various channel blockers on spontaneous firing by means of patch clamp recordings. Coronal slice (400 ㎛) of the vestibular nucleus region was sequentially treated with pronase 0.2 ㎎/㎖ and thermolysin 0.2 ㎎/㎖, then single neurons were mechanically dissociated. MVN neurons recorded in neonatal rat were shown to have either a single deep afterhyperpolarization (AHP; type A cells), or an early fast and a delayed slow AHP (type B cells). In 300 nM TTX, spontaneous firing was blocked in type B cells tested. In 8 of 11 cells, underlying fluctuation or oscillations in membrane potential was not remained, and hyperpolarization did not produce rebound low-threshold calcium spikes. Although type B MVN neurons possessed hyperpolarization activated cation current (Ih), cesium had no effect on firing rates. The spike AHP is calcium dependent. When Ca2+ influx was blocked in external Ca2+ free solution, repetitive firing was abolished and the cell rested at depolarized embrane potentials. Application of apamin (300 nM) caused a profound reduction in the amplitude of the AHP and produced rhythmic burst firing. These findings suggest that the spontaneous activity of type B MVN neurons is regulated by interactions between the membrane depolarization mainly due to a ersistent sodium conductances and hyperpolarization due to the calcium-activated potassium conductances.