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- W3201163203 endingPage "109743" @default.
- W3201163203 startingPage "109743" @default.
- W3201163203 abstract "Paroxysmal kinesigenic dyskinesia (PKD) is the most common paroxysmal dyskinesia, characterized by recurrent episodes of involuntary movements provoked by sudden changes in movement. Proline-rich transmembrane protein 2 (PRRT2) has been identified as the major causative gene for PKD. Here, we report that PRRT2 deficiency facilitates the induction of cerebellar spreading depolarization (SD) and inhibition of cerebellar SD prevents the occurrence of dyskinetic movements. Using Ca2+ imaging, we show that cerebellar SD depolarizes a large population of cerebellar granule cells and Purkinje cells in Prrt2-deficient mice. Electrophysiological recordings further reveal that cerebellar SD blocks Purkinje cell spiking and disturbs neuronal firing of the deep cerebellar nuclei (DCN). The resultant aberrant firing patterns in DCN are tightly, temporally coupled to dyskinetic episodes in Prrt2-deficient mice. Cumulatively, our findings uncover a pivotal role of cerebellar SD in paroxysmal dyskinesia, providing a potent target for treating PRRT2-related paroxysmal disorders." @default.
- W3201163203 created "2021-09-27" @default.
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- W3201163203 date "2021-09-01" @default.
- W3201163203 modified "2023-10-15" @default.
- W3201163203 title "Cerebellar spreading depolarization mediates paroxysmal movement disorder" @default.
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- W3201163203 doi "https://doi.org/10.1016/j.celrep.2021.109743" @default.
- W3201163203 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34551285" @default.
- W3201163203 hasPublicationYear "2021" @default.
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