Rescue of motor coordination by Purkinje cell-targeted restoration of Kv3.3 channels in Kcnc3-null mice requires Kcnc1.

The role of cerebellar Kv3.1 and Kv3.3 channels in motor coordination was examined with an emphasis on the deep cerebellar nuclei (DCN).

The role of Kv3-type potassium channels in cerebellar physiology and behavior.

Different subunits of the Kv3 subfamily of voltage-gated potassium (Kv) channels (Kv3.1-Kv3.4) are expressed in distinct neuronal subpopulations in the cerebellum.

Purkinje-cell-restricted restoration of Kv3.3 function restores complex spikes and rescues motor coordination in Kcnc3 mutants.

The fast-activating/deactivating voltage-gated potassium channel Kv3.3 (Kcnc3) is expressed in various neuronal cell types involved in motor function, including cerebellar Purkinje cells. Spinocerebellar ataxia type 13 (SCA13) patients carrying dominant-negative mutations in Kcnc3 and Kcnc3-null mutant mice both display motor incoordination, suggested in mice by increased lateral deviation while ambulating and slips on a narrow beam.

Isolation and culture of rat and mouse oligodendrocyte precursor cells.

The ability to isolate oligodendroglial precursor cells (OPCs) provides a powerful means to characterize their differentiation, properties and potential for myelin repair. Although much knowledge is available for isolation of OPCs from the rat central nervous system, preparation and maintenance of mouse OPCs has been until recently a challenge owing to difficulties in obtaining a sufficient quantity of purified OPCs. Here, we describe protocols to prepare highly enriched rat OPCs and nearly homogenous mouse OPCs.

A crucial role for Olig2 in white matter astrocyte development.

The mechanisms underlying astrocyte heterogeneity in the developing mouse brain are poorly understood. The bHLH transcription factor Olig2 is essential for motoneuron and oligodendrocyte formation; however, its role in astrocyte development remains obscure. During cortical development, Olig2 is transiently expressed in immature developing astrocytes at neonatal stages and is progressively downregulated in astrocytes at late postnatal stages.