Inhibition of TRPC1-dependent store-operated calcium entry improves synaptic stability and motor performance in a mouse model of huntington's disease

Abstract: Huntington disease (HD) is a dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. We previously discovered that mutant Huntingtin sensitizes type 1 inositol 1,4,5-trisphosphate receptor (InsP3R1) to InsP3. This causes calcium leakage from...

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Detalles Bibliográficos
Autores principales: Wu, Jun, Ryskamp, Daniel, Birnbaumer, Lutz, Bezprozvanny, Ilya
Formato: Artículo
Lenguaje:Inglés
Publicado: IOS Press 2019
Materias:
ENFERMEDAD DE HUNTINGTON
CALCIO
TRATAMIENTO MEDICO
PROTEINAS
LUZ
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/8701
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
Descripción
Sumario:Abstract: Huntington disease (HD) is a dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. We previously discovered that mutant Huntingtin sensitizes type 1 inositol 1,4,5-trisphosphate receptor (InsP3R1) to InsP3. This causes calcium leakage from the endoplasmic reticulum (ER) and a compensatory increase in neuronal store-operated calcium (nSOC) entry. We previously demonstrated that supranormal nSOC leads to synaptic loss in striatal medium spiny neurons (MSNs) in YAC128 HD mice.

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