Abstract
In the medial vestibular nucleus (MVN), an input-dependent influx of Ca 2+ into neurons through N- methyl- d-aspartate (NMDA) receptor-linked channels and/or voltage-dependent Ca 2+ channels is suggested as underlying certain mechanisms of plasticity of the vestibular system. To see whether there is an increase in intracellular Ca 2+ induced by afferent synaptic inputs to MVN neurons, we measured changes in [Ca 2+] i with microfluorometry using a Ca 2+ 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 Ca 2+ 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 Ca 2+ into MVN neurons due, at least in part, to the activation of NMDA receptors and the subsequent operation of L-type Ca 2+ channels in young rats.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
