The horizontal angular vestibuloocular reflex (VOR) evoked by high- frequency, high-acceleration rotations was studied in four squirrel monkeys after unilateral labyrinthectomy. Spontaneous nystagmus was measured at the beginning and end of each testing session. During the period that animals were kept in darkness (4 days), the nystagmus at each of these times measured ~20°/s. Within 18 24 h after return to the light, the nystagmus (measured in darkness) decreased to 2.8 ± 1.5°/s (mean ± SD) when recorded at the beginning but was 20.3 ± 3.9°/s at the end of the testing session. The latency of the VOR measured from responses to steps of acceleration (3,000°/s2 reaching a velocity of 150°/s) was 8.4 ± 0.3 ms for responses to ipsilesional rotations and 7.7 ± 0.4 ms for contralesional rotations. During the period that animals were kept in darkness after the labyrinthectomy, the gain of the VOR measured during the steps of acceleration was 0.67 ± 0.12 for contralesional rotations and 0.39 ± 0.04 for ipsilesional rotations. Within 18-24 h after return to light, the VOR gain for contralesional rotations increased to 0.87 ± 0.08, whereas there was only a slight increase for ipsilesional rotations to 0.41 ± 0.06. A symmetrical increase in the gain measured at the plateau of head velocity was noted after the animals were returned to light. The VOR evoked by sinusoidal rotations of 2-15 Hz, ±20°/s, showed a better recovery of gain at lower (2- 4 Hz) than at higher (6-15 Hz) frequencies. At 0.5 Hz, gain decreased symmetrically when the peak amplitude was increased from 20 to 100°/s. At 10 Hz, gain was decreased for ipsilesional half-cycles and increased for contralesional half-cycles when velocity was raised from 20 to 50°/s. A model incorporating linear and nonlinear pathways was used to simulate the data. Selective increases in the gain for the linear pathway accounted for the recovery in VOR gain for responses at the velocity plateau of the steps of acceleration and for the sinusoidal rotations at lower peak velocities. The increase in gain for contralesional responses to steps of acceleration and sinusoidal rotations at higher frequencies and velocities was due to an increase in the contribution of the nonlinear pathway. This pathway was driven into cutoff and therefore did not affect responses for rotations toward the lesioned side.
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