Motor deficits in Neurofibromatosis 1 mice: the role of the cerebellum.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.HCN channels are a novel therapeutic target for cognitive dysfunction in Neurofibromatosis type 1Intrinsic plasticity complements long-term potentiation in parallel fiber input gain control in cerebellar purkinje cells.Effect of simvastatin on cognitive functioning in children with neurofibromatosis Type 1.betaCaMKII controls the direction of plasticity at parallel fiber-Purkinje cell synapses.Motor learning in children with neurofibromatosis tyoe I.Cerebellum-dependent associative learning is not impaired in a mouse model of neurofibromatosis type 1
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Y. Elgersma