Experimental Brain Research

, Volume 82, Issue 2, pp 254–262

Actions of excitatory amino acid antagonists on synaptic inputs to the rat medial vestibular nucleus: an electrophysiological study in vitro

  • K. Doi
  • T. Tsumoto
  • T. Matsunaga
Article

DOI: 10.1007/BF00231245

Cite this article as:
Doi, K., Tsumoto, T. & Matsunaga, T. Exp Brain Res (1990) 82: 254. doi:10.1007/BF00231245

Summary

The actions of excitatory amino acid (EAA) antagonists on synaptic inputs to neurons in the rat medial vestibular nucleus (MVN) from ipsilateral vestibular afferents and vestibular commissures were studied in brain stem slice preparations. Antagonists used were 2-amino-5-phosphonovalerate (APV), a selective antagonist for the N-methyl-D-aspartate (NMDA) type of EAA receptors, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a selective antagonist for the quisqualate/kainate (non-NMDA) type of EAA receptors and kynurenate (KYNA), a broad spectrum antagonist for the three types of EAA receptors. MVN neurons were classified as having mono- or polysynaptic inputs from vestibular afferents and commissural fibers by calculating synaptic delay. An application of APV through the perfusion medium suppressed 82% of cells activated monosynaptically from commissures, while it suppressed only 9% of cells activated monosynaptically from vestibular afferents. The application of KYNA proved much less selective, suppressing 83% of the former group of cells and 93% of the latter. CNQX suppressed almost all the cells of both groups. The sensitivity of monosynaptic inputs to KYNA, CNQX or APV was not significantly different from that of polysynaptic inputs irrespective of sources of inputs. These results suggest that excitatory synaptic inputs to MVN neurons are mediated mainly through non-NMDA type of EAA receptors from vestibular afferents and through NMDA as well as non-NMDA types of EAA receptors from commissures.

Key words

NMDA receptorQuisqualate/kainate receptorExcitatory amino acidMedial vestibular nucleusSliceRat

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • K. Doi
    • 1
  • T. Tsumoto
    • 2
  • T. Matsunaga
    • 1
  1. 1.Department of OtolaryngologyOsaka University Medical SchoolOsakaJapan
  2. 2.Department of NeurophysiologyBiomedical Research Center, Osaka University Medical SchoolOsakaJapan
  3. 3.Laboratory of Molecular Otology, NIDCD, NIHBethesdaUSA
  4. 4.LMO, NIDCD, NIHBethesdaUSA