Article Figures & Data
Figures
- Figure 1.
Examples of neuronal responses to different paradigms used in the present study. A, Neurons were identified by their eye position sensitivity (top) and pauses during saccadic eye movements (arrows). B, Responses of two example neurons to whole-body rotations. Following bilateral labyrinthectomy, no responses were observed. C, Response to neck proprioceptor stimulation. Some of the neurons modulated during rotations of the body under a stationary head (i.e., neck proprioceptive stimulation), while others showed no response. D, Response to passive head-on-body rotation. Neurons with neck sensitivity were similarly modulated during passive head-on-body and body-under-head (BUH) rotations (dashed red line). Predicted responses in normal animals (blue lines) are also shown for all panels (based on values from Sadeghi et al., 2010).
- Figure 2.
Changes in neuronal responses after bilateral labyrinthectomy. A, Response of the population of PVP neurons to whole-body rotation. Vestibular sensitivities were absent after the second labyrinthectomy and did not recover at any time. Asterisks denote significant difference with regard to pre-lesion. B, Response of neurons to stimulation of neck proprioceptors. For the population of neck-sensitive neurons [i.e., sensitivity > 0.1 (spikes/s)/(°/s)]; average sensitivities increased over time after bilateral lesion. Note that the direction of neck sensitivities was accounted for in the calculation. Asterisks show significance with regard to day 1. Left inset, The proportion of neck-sensitive neurons decreased over time. Right inset, Individual neurons had comparable sensitivities during passive head-on-body and body-under-head rotations. C, Changes in the resting discharge of PVP neurons after bilateral lesion. Resting discharges were similar to normal conditions and compensated chronic stage after unilateral labyrinthectomy for up to ∼2 weeks after bilateral lesion and decreased afterward.
- Figure 3.
Development of the COR after bilateral labyrinthectomy in the absence of VOR. A, Eye movements generated during whole-body rotations 2 months after unilateral labyrinthectomy (i.e., compensated VOR) (data from Sadeghi et al., 2010) and after bilateral labyrinthectomy. VOR responses are absent following bilateral lesion even after 4 weeks. B, COR gain increased over time after bilateral labyrinthectomy. B1, Example of COR responses after bilateral labyrinthectomy. B2, At each time point after the lesion, the COR response was absent (i.e., gain < 0.1) during some of the trials even in the same session (gray solid line). When all trials were considered together, the COR gain was significantly increased after ∼1 month (dashed line). All stimuli had a frequency of 0.5 Hz. Asterisks signify significant differences compared with day 1.
- Figure 4.
Evidence of a centrally programmed signal that mediates compensatory eye movements. A, In animals fully compensated after unilateral labyrinthectomy, no compensatory eye movements were observed. Bottom trace shows the activity of neurons above the value at the beginning of eye fixation periods. B, At the early stages after bilateral lesion (week 1) still no compensatory responses were observed. C, Later in the course of compensation after bilateral lesion, compensatory eye movements were observed together with increases in the activity of PVP neurons (bottom trace). Trace labels are the same as A and B. D, For the population of neurons recorded, the centrally programmed signal increased significantly after the second week postlesion.
- Figure 5.
Comparison of average neuronal and behavioral responses during passive and active head-on-body rotations after bilateral labyrinthectomy. A, The response of example neck-sensitive and neck-insensitive PVP neurons during passive and active head-on-body rotations 4 weeks after the lesion. The schematic illustrates an efference copy signal that is potentially available during active movements. Prediction (dashed red) based on passive movements underestimates neuronal responses during active movements (black line). B, Population average of the gain of the VOR-like response and neuronal firing rates (n = 12 on day 1, 18 on week 1, 14 on week 2–3, and 21 after week 3) increased over time after the lesion. Asterisks signify significant differences compared with day 1. C, The efference copy signal estimated during active head movements and brake paradigm were comparable. Note that this analysis was completed on neuronal responses to high-velocity active and passive head movements (∼200°/s), that corresponded to the intended (but unrealized) movements during the brake paradigm.
- Figure 6.
Time course of dynamic regulation of multimodal integration following bilateral labyrinthectomy. Responses are normalized relative to the maximum response to each of the three inputs: vestibular (blue, measured by whole-body rotation), neck proprioceptive (red, measured by body-under-head rotation), and preprogrammed/efference copy signal (green, measured by the brake paradigm and active head movements). Vestibular inputs are lost immediately after bilateral lesion. Over the weeks following the lesion, contribution of neck signals increased in about 2–3 weeks. Over the same time period, responses of PVP neurons were enhanced by a preprogrammed/efference copy signal from higher brain areas during actively generated movements.
