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Una subunidad β del canal de potasio acopla el transporte de electrones mitocondriales al sueño

Anissa Kempf¹, Seoho M Song¹, Clifford B Talbot¹

¹Centre for Neural Circuits and Behaviour, University of Oxford, Oxford, UK.

|March 22, 2019

Resumen

La pérdida de sueño aumenta el estrés oxidativo en las células cerebrales de la mosca de la fruta, alterando una proteína clave para promover el sueño. Este descubrimiento vincula mecánicamente el metabolismo energético, el estrés oxidativo y la regulación del sueño.

Área de la Ciencia:

La neurociencia
Biología molecular
El metabolismo

Sus antecedentes:

Las funciones esenciales del sueño están vinculadas a cambios moleculares en los sistemas de control del sueño.
En Drosophila, las neuronas que inducen el sueño en el dFB regulan la salida eléctrica basada en la necesidad de sueño a través de las conductancias de potasio.

Objetivo del estudio:

Investigar los mecanismos moleculares por los cuales los subproductos oxidativos regulan la actividad neuronal y el sueño.
Para aclarar el papel de la proteína hipercinética y su cofactor de nicotinamida adenina dinucleótido fosfato (NADPH) en la regulación del sueño.

Principales métodos:

Investigó la regulación de la subunidad K_Vβ de Shaker, Hipercinética, por subproductos oxidativos mitocondriales en las neuronas Drosophila dFB.
Examinó el efecto de la pérdida de sueño en las especies de oxígeno reactivo mitocondrial y la relación NADP + NADPH en las neuronas dFB.
Se evaluó el impacto de la oxidación del cofactor en la frecuencia de activación de la corriente de tipo A y el potencial de acción.

Principales resultados:

Los subproductos oxidativos del transporte de electrones mitocondriales regulan la actividad de las neuronas dFB a través del cofactor NADPH de Hyperkinetic.
La pérdida de sueño eleva las especies de oxígeno reactivo mitocondrial, lo que lleva a la conversión de Hyperkinetic a la forma ligada a NADP.
La oxidación del cofactor retrasa la inactivación de la corriente de tipo A y aumenta la frecuencia del potencial de acción, promoviendo el sueño.

Conclusiones:

El metabolismo energético, el estrés oxidativo y el sueño están interconectados mecánicamente.
La proporción de NADPH ligado a NADP+ en hipercinético sirve como un registro molecular de la deuda de sueño o tiempo de vigilia.
Los sustratos K_Vβ o los inhibidores que alteran esta relación son prototipos potenciales para los medicamentos reguladores del sueño.

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