Purkinje cell collaterals regulate processing in the input layer of the cerebellum by providing fast stochastic GABA_A-mediated and slow GABA_B-mediated inhibition to a specialized subset of unipolar brush cells.

Computational and theoretical models show that rate adaptation of phase responses can regulate Purkinje cell outputs by forming transient oscillations in fast-spiking neurons.

Physiological and behavioral analyses show that expression of cerebellar whisker learning can be mediated by increased simple spike activity, depending on LTP induction at parallel fiber to Purkinje cell synapses.

Tsc1 mutation in cerebellar Purkinje cells leads to downregulation of synapse genes that are targets of the Fragile X Mental Retardation Protein.

Purkinje cell-specific ablation demonstrates regeneration of these neurons and functional recovery of the cerebellum during both larval and adult zebrafish.

Intersectional genetics show that excitatory neurons are essential for the functional and anatomical maturation of cerebellar circuits in mice.

Purkinje cells of the cerebellum, a conserved vertebrate brain region important for sensorimotor integration, receive sensory and motor information from distinct input streams and are functionally clustered into modules reflecting the larval zebrafish's behavioral repertoire.

Electrophysiological analysis and imaging in live zebrafish reveal that infant- and adult-onset SCA13 mutations have distinct effects on the electrical activity, development, and survival of cerebellar Purkinje cells.

Genetic, pharmacologic, and optogenetic manipulations demonstrate that Purkinje cells can trigger and propagate the signals for tremor.

Different Purkinje cell subpopulations show distinct developmental profiles of physiological activity, climbing fiber inputs and axonal and dendritic morphology, matching different timelines of cerebellum-dependent behaviors.