Cerebellar control of vestibulo-ocular reflex (VOR) studied with injection of harmaline in the trained baboon
Gauthier, G.M.; Marchetti, E.; Pellet, J.
Archives Italiennes de Biologie 121(1): 19-36
1983
ISSN/ISBN: 0003-9829 PMID: 6601938 Document Number: 215668
Harmaline (H) activates the inferior olive cells projecting via the climbing fiber pathway to the cerebellar cortex. The effects of the drug on the cerebellar control of the vestibulo-ocular reflex gain (VORG) was studied in 4 adult monkeys (P. papio) trained to fixate visual targets. In the normal monkey the VORG measured in total darkness was in a range 0.84-0.96 at a frequency of 0.3 Hz and close to unity at 0.1 Hz. After injection of 3 mg/kg of H, numerous intrusive saccades altered the pattern of the nystagmogram, but on the average the VORG remained constant. When the normal animals were rotated before a stationary visual target the VORG was unity. Five minutes after H-injection, the slow compensatory eye movements lost their regularity, and large amplitude refixation and intrusive saccades were observed. The VORG was still unity. When the animals fixed a visual target rotating with the turntable in a normal situation, the VORG was close to zero. The eye position was very steady except for very small amplitude saccades. After H-injection, fixation was altered by large fixation saccades and intrusive saccades. The eye movement velocity signal showed a definite modulation at the head rotation frequency. After a 3 mg/kg injection, the mean VORG was 0.2 .+-. 0.1. With higher doses of the drug, the modulation of the eye velocity signal increased. When the animals were rotated before a stationary visual target seen through a magnifying lens (.times. 2), the eye movement amplitude increased to twice that of the head. Small amplitude saccades were superposed on the otherwise smooth eye movement pattern. When the target was turned off the VORG decreased to unity after 200-300 ms. After a 3 mg/kg of H injection, the eye movement velocity was lower than twice that of the head and numerous refixation and large amplitude intrusive saccades appeared. When the uninjected animals were rotated with a mobile target seen through the magnifying lens, the fixation performance was similar to that realized in the normal viewing situation: the VORG was close to zero. After administration of 3 mg/kg of H, eye movement fixation was very much altered. Numerous intrusive saccades were generated and a definite modulation of the slow component of eye movements resulted, which meant that the VOR was not completely suppressed. When the animals were rotated at 0.3 Hz over a long period of time before a stationary visual target seen through the magnifying lens, the VORG increased continuously by as much as 30% after 30-40 min. Injected with low doses of H, the animals showed little adaptation. With 8 mg/kg, the adaptation was abolished. H altered the saccadic eye movement control by generating intrusive saccades during fixation and smooth ocular movements. It also altered the mechanisms responsible for suppression (mobile target) and enhancement (stationary target) of the VOR and prevented VOR adaptation to a magnifying lens. The results are interpreted in the light of recent knowledge and hypotheses regarding the possible involvement of the cerebellum in both the adaptative control of the VORG and in the compensation of the VOR in situations where the visual target rotates with the head.