Molecular mechanisms of recovery from vestibular damage in mammals: recentadvances

The aim of this review is to summarise and critically evaluate studies of v estibular compensation published over the last 2 years, with emphasis on th ose concerned with the molecular mechanisms of this process of lesion-induc ed plasticity. Recent studies of vestibular compensation have confirmed and extended the previous findings that: (i) compensation of the static ocular motor and postural symptoms occurs relatively rapidly and completely compa red to the dynamic symptoms, many of which either do not compensate substan tially or else compensate variably due to sensory substitution and the deve lopment of sensorimotor strategies which suppress or minimize symptoms; (ii ) static compensation is associated with, and may be at least partially cau sed by a substantial recovery of resting activity in the ipsilateral vestib ular nucleus complex (VNC), which starts to develop very quickly following the unilateral vestibular deafferentation (UVD) but does not correlate perf ectly with the development of some aspects of static compensation (e.g., po stural compensation); and (iii) many complex biochemical changes are occurr ing in the VNC, cerebellum and even areas of the central nervous system lik e the hippocampus, following UVD. However, despite many recent studies whic h suggest the importance of excitatory amino acid receptors such as the N-m ethyl-D-aspartate receptor, expression of immediate early gene proteins, gl ucocorticoids, neurotrophins and nitric oxide in the vestibular compensatio n process, how these various factors are linked and which of them may have a causal relationship with the physiological changes underlying compensatio n, remains to be determined. (C) 2000 Elsevier Science Ltd. All rights rese rved.