Learning Rules for the Recruitment of Cerebellar Plasticity Mechanisms
Jennifer L. Raymond
Stanford University School of Medicine, USA
Much of the work on cerebellum-dependent learning has focused on a single plasticity mechanism, long-term depression of the synapses between parallel fibers and Purkinje cells (cerebellar LTD). However in vitro studies have reported plasticity at many of the synapses in the cerebellum and related circuitry. Are all of these plasticity mechanisms contributing to cerebellum-dependent learning? Or does cerebellar LTD play a central role, with the other plasticity mechanisms in the cerebellar circuitry playing a secondary role or perhaps no role at all in adult learning? Our studies of motor learning in the vestibulo-ocular reflex (VOR) address these questions. I’ll present several lines of evidence that 1) multiple plasticity mechanisms contribute to motor learning in the VOR, and 2) different subsets of the plasticity mechanisms present in the VOR circuit are recruited, depending on the parameters of the training paradigm.
First, behavioral studies have revealed a number of behavioral differences between changes in the VOR induced with different training paradigms. Second, mutants deficient in particular plasticity mechanisms at the synapses from parallel fibers to Purkinje cells exhibit deficits that are highly specific to particular components of motor learning in the VOR—increases vs. decreases in VOR gain, high- vs. low-frequency training, gain vs. phase adaptation. Third, the patterns of gene expression present in the medial vestibular nucleus after learning support the idea that this is a locus involved in motor memory storage. Finally, an analysis of the neural instructive signals available to guide the induction of plasticity during different training paradigms is providing insight about why particular plasticity mechanisms are recruited by some training paradigms and not others.