Synaptic input-induced increase in intraneuronal Ca2+ in the medial vestibular nucleus of young rats

In the medial vestibular nucleus (MVN), an input-dependent influx of Ca2+ into neurons through N-methyl-D-aspartate (NMDA) receptor-linked channels and/or voltage-dependent Ca2+ channels is suggested as underlying certain mechanisms of plasticity of the vestibular system. To see whether there is an increase in intracellular Ca2+ induced by afferent synaptic inputs to MVN neurons, we measured changes in [Ca2+]i with microfluorometry using a Ca2+ indicator, rhod-2, following electrical stimulation of ipsilateral vestibular afferents and commissural fibers in slice preparations of the brainstem of young rats (4-7 days postnatal). Single shock stimulation of ipsilateral afferents or commissural fibers induced an increase in fluorescence intensity lasting for several seconds. An application of 2-amino-5-phosphonovaleric acid (APV), an antagonist of NMDA receptors, almost completely blocked this stimulus-induced rise in fluorescence intensity. Nifedipine, an L-type Ca2+ channel blocker, also reduced the stimulus-induced rise in fluorescence intensity to 44-51% of the control value. These results suggest that synaptic inputs from the afferent and commissural pathways induce an influx of Ca2+ into MVN neurons due, at least in part, to the activation of NMDA receptors and the subsequent operation of L-type Ca2+ channels in young rats.