The cerebellum allows us to rapidly adjust motor behavior to the needs of the situation. It is commonly assumed that cerebellum-based motor learning is guided by the difference between the desired and the actual behavior, i.e., by error information. Not only immediate but also future behavior will benefit from an error because it induces lasting changes of parallel fiber synapses on Purkinje cells (PCs), whose output mediates the behavioral adjustments. Olivary climbing fibers, likewise connecting with PCs, are thought to transport information on instant errors needed for the synaptic modification yet not to contribute to error memory. Here, we report work on monkeys tested in a saccadic learning paradigm that challenges this concept. We demonstrate not only a clear complex spikes (CS) signature of the error at the time of its occurrence but also a reverberation of this signature much later, before a new manifestation of the behavior, suitable to improve it.
Fig1B
Eye and visual target traces
Fig1C
Trial-By-Trial saccadic adaptation
Fig1D
Normalized Trial-By-Trial adaptation
Fig2A
Complex Spike activity per direction and resulting Mutual Information between Complex Spike occurence and saccade direction
Fig2B
Directional Complex Spike preference
Fig2C
Timing of maximal Mutual Information
Fig3A
Complex Spike activity and Mutual Information between Complex Spike occurence in trial n and error condition in trial n-1
Fig3B
Trial-By-Trial adaptation
Fig3C
Timing of maximal Mutual Information for Trial-By-Trial adaptation
Fig4B
Correlation coefficients of the size of visual error in trial n-1 on the average CS activity during the significant MI interval in the primary error period of trial n.
Fig4D
Complex Spike density functions prior to primary saccade onset in trial n for the three different error conditions (outward, inward, no error) in trial n-1. Separated according to the correlation in Fig4B.
S2Fig
Total and significant datasets for each subject
S3Fig
Negative control of Fig 1D
S4Fig
Negative Control of Fig 1D of trial n-2 to trial n.
S5Fig
Directional MI analysis for the exemplary unit presented in Fig 2
S6FigA
Example for the dependency of Mutual Information on the point of alignment
S7Fig
Effect of Trial-By-Trial adaptation for directions with significant Mutual Information modulation
S8Fig
Correlation of CS activity in trial n and saccade amplitude in trial n
S9Fig
Timing of significant SS modulation analogous to Fig 3C
S10FigA
Well isolated Complex Spike and Simple Spike recording from the Purkinje Cell layer.
S10FigB
Example of Complex Spike observed in isolation from Simple Spikes, arguably recorded further away from the cell body in the molecular layer.
S10FigC
Example of a less well isolated Purkinje cell.
S10FigD
Example of the number of spikelets per Complex Spike unit as function of its duration.
S11FigA
Mean Complex Spike duration for the short (2 ms to 7 ms), the medium (3 ms to 8 ms) and the long (3 ms to 12 ms) Complex Spike durations.
S11FigB
Average CS duration for the four trial periods distinguished
S11FigC
Duration of CS fired during baseline fixation as function of duration of the same CS unit when generated in the presence of a secondary visual error.
S11FigD
Change of saccade amplitude from trial n-1 to trial n as function of Complex Spike duration in the secondary visual error interval of Fig 1B in trial n-1.
S12Fig
Simple Spike density functions prior to primary saccade onset in trial n for the three different error conditions (outward, inward, no error) in trial n-1. Separated according to the correlation in Fig4B.