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Regulación gradual del canal de potasio Kv2.1 mediante fosforilación variable
Kang-Sik Park1, Durga P Mohapatra, Hiroaki Misonou
1Department of Pharmacology, School of Medicine, University of California, Davis, CA 95616, USA.
Science (New York, N.Y.)
|August 19, 2006
Resumen
La plasticidad neuronal se basa en la fosforilación de los canales iónicos. La calcineurina desfosforila los canales de potasio Kv2.1, regulando la excitabilidad neuronal y las propiedades de disparo a través de cambios graduales en la activación del canal.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología Molecular Biología Molecular
- Fisiología del canal iónico Fisiología del canal iónico
Sus antecedentes:
- La plasticidad neuronal, la capacidad del cerebro para adaptarse, está modulada dinámicamente por la fosforilación del canal iónico.
- Los canales de potasio Kv2.1 están significativamente fosforilados en las neuronas de mamíferos en reposo, lo que influye en su función.
Objetivo del estudio:
- Investigar el papel de la fosforilación y desfosforilación de los canales de potasio Kv2.1 por la calcineurina en la regulación de la excitabilidad neuronal.
- Identificar sitios específicos de fosforilación en Kv2.1 regulados por la calcineurina y su impacto funcional.
Principales métodos:
- Utilizó el etiquetado de isótopos estables de espectrometría de masas con aminoácidos en cultivo celular (MS-SILAC) para identificar los sitios de fosforilación Kv2.1.
- Mutagénesis dirigida en el sitio empleada (sustituciones de alanina y aspartato) para imitar o bloquear la desfosforilación mediada por calcineurina.
- Se evaluaron las consecuencias funcionales de estas mutaciones en la apertura del canal Kv2.1 y la excitabilidad neuronal.
Principales resultados:
- Se identificaron 16 sitios de fosforilación Kv2.1, de los cuales 7 se encontraron desfosforilados por calcineurina.
- Las mutaciones de sitios individuales a la alanina indujeron cambios incrementales en la activación del canal, imitando la desfosforilación.
- Las mutaciones en múltiples sitios demostraron efectos aditivos, lo que indica una regulación gradual de la función del canal Kv2.1.
Conclusiones:
- La desfosforilación dependiente de la actividad de Kv2.1 por la calcineurina causa cambios graduados hiperpolarizantes en la activación, suprimiendo la excitabilidad neuronal.
- La fosforilación variable de Kv2.1 en numerosos sitios permite una regulación ajustada y dependiente de la actividad de las propiedades de disparo neuronal.
- Este mecanismo dependiente de la fosforilación proporciona una forma sofisticada de controlar la excitabilidad y plasticidad neuronales.
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