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La activación del canal catiónico TRPC1 por el receptor metabotrópico del glutamato mGluR1
Sang Jeong Kim1, Yu Shin Kim, Joseph P Yuan
1Department of Neuroscience, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, Maryland 21205, USA.
Nature
|November 14, 2003
Resumen
Los receptores metabotrópicos de glutamato del grupo I (mGluR) activan una conductividad postsináptica excitatoria lenta (EPSC) a través del canal catiónico TRPC1. Este hallazgo revela TRPC1
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología Molecular Biología Molecular
- La señalización celular.
Sus antecedentes:
- Los receptores metabotrópicos de glutamato del grupo I (mGluR) son receptores acoplados a la proteína G que participan en la plasticidad neuronal y el aprendizaje.
- Tras la activación por ráfagas de actividad, los mGluR del grupo I activan vías de señalización, incluida la estimulación de la fosfolipasa C y una lenta conductancia postsináptica excitatoria (EPSC).
- La identidad molecular del canal mediador de la EPSC lenta evocada por mGluR1 seguía siendo desconocida.
Objetivo del estudio:
- Para identificar el canal catiónico responsable de la conductividad postsináptica excitatoria lenta evocada por mGluR1.
- Investigar el papel de TRPC1 en la mediación de la transmisión sináptica en la sinapsis de células de Purkinje de fibra paralela cerebelosa.
Principales métodos:
- Registros electrofisiológicos en células de Purkinje para medir las corrientes sinápticas.
- Investigando la asociación física entre mGluR1 y TRPC1.1.
- Reconstitución funcional de la señalización de mGluR1 y TRPC1 en un sistema de expresión heterólogo.
Principales resultados:
- El estudio identificó el canal catiónico TRPC1 como el mediador de la EPSC lenta evocada por mGluR1.
- TRPC1 se expresa en regiones perisinápticas y se asocia físicamente con mGluR1 en la sinapsis celular paralela de fibra-Purkinje.
- El bloqueo de la función TRPC1 abolió la EPSC lenta evocada por mGluR1 sin afectar la transmisión rápida mediada por el receptor AMPA.
- La coexpresión de mGluR1 y TRPC1 en un sistema heterólogo reconstituyó con éxito la EPSC lenta evocada por mGluR1.
Conclusiones:
- Los canales catiónicos TRPC1 son componentes esenciales de la vía de señalización activada por mGluR1.1.
- Este hallazgo aclara un mecanismo molecular clave subyacente a la transmisión sináptica mediada por mGluR1 y la plasticidad neural.
- TRPC1 representa un objetivo terapéutico potencial para las condiciones que implican la disfunción de mGluR1.
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