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In contrast, during VOR-decrease training, there was no trial-by-trial correlation between climbing fiber activity and changes in cerebellar output, and climbing fiber activation did not induce VOR-decrease learning.
At the same time, dendrites of different Purkinje cells showed increased co-activation, reflecting increased synchrony of climbing fiber activity.
Most subsequent cerebellar-learning models, however, have followed Albus in assuming that climbing fiber activity would be an error signal, and would cause synchronously activated parallel fiber inputs to be weakened.
In this study, we describe a second level of regulation in animals undergoing learning: even when climbing fibers are robustly activated by performance errors, the ability of that climbing fiber activity to trigger plasticity can be regulated by the state of the cerebellar circuit.
In contrast with anesthetized recordings, no 1-10 Hz oscillations in climbing fiber activity were evident.
Mossy fibers are random spike generators. of mossy fiber activity are variable parameters.
The model predicts that, under conditions of strong mossy fiber input to the cerebellum, Golgi cells do not only control the strength of parallel fiber activity but also the timing of the individual spikes.
Climbing fiber activity could guide learning during all stimuli tested but only if compared with the activity present approximately 100 msec earlier in either vestibular pathways or Purkinje cells.
In the case of cerebellum, we have identified a learning rule that favors parallel fiber activity that leads the complex spike by tens to hundreds of milliseconds, consistent with order-dependent learning seen in vivo.
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Either there are multiple mechanisms of learning that use different combinations of neural signals to drive plasticity, or there is a single mechanism tuned to climbing-fiber activity that follows activity in vestibular pathways by approximately 100 msec.
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