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• W2097063303 abstract "Purkinje neurons are the sole output neuron of the cerebellar cortex, and they generate high-frequency action potentials. Electrophysiological dysfunction of Purkinje neurons causes cerebellar ataxia. Mutant med mice have the lack of expression of the Scn8a gene. This gene encodes the NaV1.6 protein. In med Purkinje neurons, regular high-frequency firing is slowed, and med mice are ataxic. The aim of this study was to propose the neuroprotective drugs which could be useful for ataxia treatment in med mice, and to investigate the neuroprotective effects of these drugs by simulation. Simulation results showed that Kv4 channel inhibitors and BK channel activators restored the normal electrophysiological properties of the med Purkinje neurons. 4-Aminopyridine (4-AP) and acetazolamide (ACTZ) were proposed as neuroprotective drugs for Kv4 channel inhibitor and BK channel activator, respectively." @default.
• W2097063303 created "2016-06-24" @default.
• W2097063303 creator A5037275437 @default.
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• W2097063303 date "2014-02-01" @default.
• W2097063303 modified "2023-09-26" @default.
• W2097063303 title "Introducing treatment strategy for cerebellar ataxia in mutant med mice: Combination of acetazolamide and 4-Aminopyridine" @default.
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• W2097063303 doi "https://doi.org/10.1016/j.cmpb.2013.11.008" @default.
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• W2097063303 hasPublicationYear "2014" @default.
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