In a previous in vitro study, we have shown that guinea-pig medial vestibular nucleus neurons (MVNn) can be grouped into two main cell types based on their intrinsic membrane properties. Subsequent in vivo and in vitro studies demonstrated that these neurons are endowed with N-methyl-D-aspartate (NMDA) receptors and that NMDA induces rhythmic bursts in B MVNn. We now report the occurrence of rhythmic bursts in B MVNn (and in the subclass of B+LTS MVNn) which are induced by long-lasting perfusion of either apamin, a selective blocker of one type of Ca(2+)-dependent K+ conductance (SK channels), or by a high Mg2+/low Ca2+ artificial cerebrospinal fluid. Apamin-induced bursts were studied in vitro in brainstem slices, and in vivo in the alert unrestrained guinea-pig. In vitro, intracellular recordings demonstrated that the frequency of the bursts was voltage dependent. These bursts were insensitive to D-2-amino-5-phosphopentanoic acid but could be abolished by tetrodotoxin or blocked by the bath application of 20-50 microM of ouabain, a blocker of the sodium pump. In the in vivo preparation, unilateral infusion of apamin into the vestibular nuclei induced oscillatory head and eye movements. Our data show that the blockade of a Ca(2+)-activated K+ conductance may switch, in vitro and probably in vivo, the B MVn firing pattern from a regular to a bursting firing pattern.