Fifteen hundred and thirty cells were recorded in the medial vestibular nucleus (MVN) of alert monkeys whose vestibuloocular reflex (VOR) had been adapted to one of two kinds of spectacles. The "high-gain" sample was recorded from monkeys that had worn 2.0 x telescopic spectacles; the gain of the VOR in the dark (eye velocity divided by head velocity) was greater than 1.5. The "low-gain" sample was recorded from monkeys that had worn goggles providing a visual field that was fixed with respect to the freely turning head; the gain of the VOR was less than 0.4. 2. Cells showing modulation of firing rate related to imposed head velocity were grouped into four categories: pure vestibular (10), vestibular-plus-saccade (10), vestibular-plus-position (10), and vestibular-plus-head/body (24). Sensitivity to head velocity was measured from averaged responses to sinusoidal, 0.4-Hz whole-body oscillation in the horizontal plane. Almost all cells (98%) having increased firing during ipsilateral head rotation received inputs from the horizontal semicircular canals. Conversely, 82% of cells having increased firing during contralateral head rotation received inputs from the vertical canals. 3. There were no statistically significant differences in resting discharge rate, phase shift, or sensitivity to head velocity between the high- and low-gain samples of any of the cell types. Nonetheless, there was a consistent tendency, evident in all the functionally defined cell groups, for the sensitivity to be about 20% greater in the high-gain samples. However, this difference is small by comparison with the fourfold difference in VOR gain. 4. Detailed scrutiny of the response properties of individual cells suggested that the small differences in sensitivity reflect small changes distributed throughout the population, rather than large and potentially significant changes within a small sub-population. 5. Our data indicate that large, adaptive changes in the gain of the VOR are accompanied by only minor changes in the vestibular sensitivity and no changes in the phase shift or resting discharge rates of cells in the MVN. It remains possible that large changes in vestibular sensitivity occurred in cells we did not sample or in subgroups we could not identify. We argue that this is unlikely and that the major changes underlying VOR plasticity occur after the first central synapse in the VOR pathways.
