THE CONTRIBUTION OF N-METHYL-D-ASPARTATE RECEPTORS TO LESION-INDUCED PLASTICITY IN THE VESTIBULAR NUCLEUS

The aim of this paper is to: i) review the behavioural, electrophysiol ogical, pharmacological and biochemical evidence relating to the invol vement of N-methyl-D-aspartate (NMDA) receptors in the vestibular comp ensation process which follows unilateral peripheral vestibular deaffe rentation (UVD); and ii) suggest a unifying hypothesis based on this l iterature and recent studies of long-term depression (LTD)-like phenom ena in the brainstem vestibular nucleus complex (VNC). It is suggested that NMDA receptors may induce a form of heterosynaptic LTD in the ip silateral VNC, which is partly responsible for the extent of the hypoa ctivity which occurs immediately following UVD, and the severity of th e associated vestibular syndrome. It is also suggested that vestibular compensation may develop as this LTD dissipates, allowing remaining s ynaptic inputs and the intrinsic properties of ipsilateral VNC neurons to re-establish the resting activity which is responsible for static vestibular compensation. It is argued that this hypothesis accounts fo r the majority of the available data on NMDA receptors in relation to vestibular compensation, and may serve as a useful working hypothesis, in order to formulate further experiments to investigate the contribu tion of NMDA receptors to the compensation process. (C) 1997 Elsevier Science Ltd.