The transmission of vestibular inputs to reticulospinal (RS) neurones of the posterior rhombencephalic nucleus (PRRN) has been shown to be depressed by the bath application of N-methyl-D-aspartate (NMDA). The aim of this study was to investigate the pharmacological mechanism involved using patch clamp recordings of reticulospinal neurones. It is demonstrated that the chemical component of vestibular inputs to the PRRN is mediated by glutamatergic synapses utilising alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors on the PRRN neurones. Monosynaptic excitatory postsynaptic currents (EPSCs) from octavomotorius relay cells to RS neurones are markedly depressed by the application of NMDA, a depression which was insensitive to competitive and non-competitive NMDA receptor antagonists. The effect of NMDA was eliminated by inactivation of G proteins. A similar depressive effect was observed following application of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) to the superfusate. It is concluded that NMDA acts at a metabotropic receptor located most likely presynaptically to reticulospinal neurones on terminals of octavomotorius relay cells.