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Synaptic transmission and plasticity at inputs to murine cerebellar purkinje cells are largely dispensable for standard nonmotor tasks.Purkinje cell-specific knockout of the protein phosphatase PP2B impairs potetiation and cerebellar motor learning.Stress, caffeine and ethanol trigger neurological dysfunction through shared mechanisms in a mouse calcium channelopathy.Cerebellar ataxia by enhanced CaV2.1 curents is alleviated by Ca2+-dependent K+-channel activators Cacna1aS218L mutant mice.Spatiotemporal firing patterns in the cerebellum.Silencing the majority of cerebellar granule cells uncovers their essential role in motor learning and consolidation.Climbing fiber input shapes reciprocity of Purkinje cell firing.Reevaluating the role of LTD in cerebellar motor learning.Synaptic inhibition of Purkinje cells mediates consolidation of vestibulo-cerebellar motor learning.STD-dependent and independent encoding of input irregularity as spike rate in a computational model of a cerebellar nucleus neuron.Purkinje cell-specific ablation of Ca(V)2.1 channels is sufficient to cause cerebellar ataxia in mice.High frequency burst firing of granule cells ensures transmission at the parallel fiber to purkinje cell synapse at the cost of temporal coding.betaCaMKII controls the direction of plasticity at parallel fiber-Purkinje cell synapses.Anatomical investigation of potential contacts between climbing fibers and cerebellar golgi cells in the mouse.Causes and consequences of oscillations in the cerebellar cortex.Differential olivo-cerebellar cortical control of rebound activity in the cerebellar nuclei.High cortical spreading depression susceptibility and migraine-associated symptoms in Ca(v)2.1 S218L mice.The cerebellar nuclei take center stage.
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F.E. Hoebeek