Comput Methods Programs Biomed - Introducing treatment strategy for cerebellar ataxia in mutant med mice: combination of acetazolamide and 4-aminopyridine.

Tópicos

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Resumo

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.

Resumo Limpo

purkinj neuron sole output neuron cerebellar cortex generat highfrequ action potenti electrophysiolog dysfunct purkinj neuron caus cerebellar ataxia mutant med mice lack express scna gene gene encod nav protein med purkinj neuron regular highfrequ fire slow med mice atax aim studi propos neuroprotect drug use ataxia treatment med mice investig neuroprotect effect drug simul simul result show kv channel inhibitor bk channel activ restor normal electrophysiolog properti med purkinj neuron aminopyridin ap acetazolamid actz propos neuroprotect drug kv channel inhibitor bk channel activ respect

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