Spontaneous Saccades and Gaze‐Holding Ability in the Pigmented Rat. II. Effects of Localized Cerebellar Lesions

Abstract

We have studied the effects of the ablation of the cerebellar vermal area corresponding to lobules VI - VIII and of the flocculus - paraflocculus of both sides on the spontaneous eye movements performed in the light and in the dark in head-restrained pigmented rats. These effects have been compared with those already described for the inferior olive lesion. The cerebellar lesions were performed 1 week to 6 months in advance. Eye movements were recorded through a phase detection search coil apparatus. Following vermal topectomy, the main characteristics of the spontaneous saccades are unmodified. Following the ablation of the flocculus - paraflocculus there is no change in the saccadic main sequence. However, the spontaneous saccades in the dark present a postsaccadic drift made up of two components with different time courses, the first one being fast and the second one slow. The former is due in part to a mismatch between the phasic (the pulse) and the tonic (the step) components of the eye movements; the latter to the leakage of the neural integrator. In light only the first component is present and the eye maintains a steady position. The time constant of the neural integrator is considerably reduced to approximately 600 - 900 ms from a value of approximately 1600 - 4000 ms in the intact rats. The amplitude of the postsaccadic drift in the light depends on both the mismatch between the pulse and the step of innervation of the extraocular muscles and the increased leakiness of the neural integrator. The gain of the pulse to step transformation is reduced to approximately 0.79 at all saccadic amplitudes and eccentricities and such a reduction is due to a decreased step amplitude, while the pulse amplitude remains unchanged. The contribution of the leakage of the neural integrator to the postsaccadic drift in the light is a function of the eccentricity with a slope of 0.23. The deficits described after flocculus - paraflocculus ablation are also very similar to those described following inferior olive lesion from a quantitative point of view. The possible mechanisms of the visually activated olivocerebellar system in the control of saccadic performance and in maintaining its calibration are discussed.

Bifurcation theory explains waveform variability in a congenital eye movement disorder

“…The constant β is the weight of the reciprocally inhibitory connections between VUs. In the absence of the cerebellum the time-constant for the integrator is reduced from about 20s to about 1s in primates (Zee et al 1981), and from about 2s to under 1s in rodents (Chelazzi et al 1990). To demonstrate the robustness of the model, we choose β to give a time-constant for the integrator of 0.2s in the absence of PCs (β = 0.348).…”

“…The PCs represent Purkinje cells in the floccular complex of the cerebellum. Lesions of these structures cause profound integrator deficits (Cannon and Robinson 1987;Zee et al 1981;Chelazzi et al 1990). With a normal, intact cerebellum, integrator time constant and gain are independently adjustable (Tiliket et al 1994).…”

Using input minimization to train a cerebellar model to simulate regulation of smooth pursuit

“…The eye position signal is generated by the brainstem neural integrator in concert with the floccular complex (Zee et al 1981;Chelazzi et al 1990). The dynamics of this interaction are complex (e.g., Anastasio and Gad 2007;Barreiro et al 2008) and beyond the focus of this study.…”

Sparse cerebellar innervation can morph the dynamics of a model oculomotor neural integrator

“…Lesions of the flocculus and ventral paraflocculus (referred to as the floccular complex) abolish VOR plasticity (Robinson, 1976;Nagao, 1983;Godaux and Vanderkelen, 1984;Rambold et al, 2002;Nagao and Kitazawa, 2003) and reduce the integrator time constant to a baseline value (Robinson, 1974;Zee et al, 1981;Chelazzi et al, 1990). Mice with genetic abnormalities of the cerebellum also show integrator deficits (Stahl and James, 2005) and reduced VOR plasticity (Stahl, 2004;Katoh et al, 2005).…”