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, electrophysiological, pharmacological and biochemical evidence relating to the involvement of N-methyl-D-aspartate (NMDA) receptors in the vestibular compensation process which follows unilateral peripheral vestibular deafferentation (UVD); and ii) suggest a unifying hypothesis based on this literature and recent studies of long-term depression (LTD)-like phenomena in the brainstem vestibular nucleus complex (VNC). It is suggested that NMDA receptors may induce a form of heterosynaptic LTD in the ipsilateral VNC, which is partly responsible for the extent of the hypoactivity which occurs immediately following UVD, and the severity of the associated vestibular syndrome. It is also suggested that vestibular compensation may develop as this LTD dissipates, allowing remaining synaptic 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 for 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 contribution of NMDA receptors to the compensation process.