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La neurotransmisión en miniatura estabiliza la función sináptica a través de la supresión tónica de la síntesis de
Michael A Sutton1, Hiroshi T Ito, Paola Cressy
1Division of Biology 114-96, California Institute of Technology, Pasadena, CA 91125, USA.
Cell
|May 23, 2006
Resumen
El escalamiento homeostático en las neuronas es más rápido de lo que se pensaba. El bloqueo de la actividad del receptor NMDA (NMDAR) durante eventos sinápticos en miniatura aumenta rápidamente la fuerza sináptica al alterar la expresión de proteínas localmente en las dendritas.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- La plasticidad sináptica.
- Biología Molecular Biología Molecular
Sus antecedentes:
- La privación de la actividad neuronal desencadena el escalado homeostático para estabilizar la función de la red.
- Investigaciones anteriores enfatizaron el papel de la transmisión impulsada por el potencial de acción (PA) en la homeostasis sináptica.
Objetivo del estudio:
- Investigar el papel de la transmisión sináptica en miniatura en el escalamiento homeostático.
- Determinar los mecanismos subyacentes a la rápida escalación sináptica inducida por el bloqueo del receptor NMDA (NMDAR).
Principales métodos:
- Utilizó el bloqueo AP para aislar la transmisión sináptica en miniatura.
- Antagonistas NMDAR administrados para bloquear eventos sinápticos en miniatura.
- Se evaluaron los cambios en la fuerza sináptica, la expresión superficial de GluR1 y la incorporación del receptor AMPA.
- Investigó el requisito para la síntesis de proteínas dendríticas locales.
Principales resultados:
- La transmisión sináptica en miniatura influye significativamente en la velocidad y el mecanismo de escalado homeostático.
- Breve bloqueo NMDAR rápidamente aumentó la fuerza sináptica, órdenes de magnitud más rápido que el bloqueo AP solo.
- El escalamiento rápido implicó un aumento de la GluR1 superficial y una inserción transitoria del receptor AMPA Ca2+ permeable.
- Estos cambios sinápticos ocurrieron localmente en las dendritas y requirieron la síntesis de proteínas.
Conclusiones:
- La señalización del receptor NMDA (NMDAR) durante la transmisión sináptica en miniatura suprime activamente la síntesis de proteínas dendríticas.
- Esta supresión normalmente limita la escala sináptica, lo que sugiere que los NMDAR estabilizan la función sináptica al inhibir la plasticidad homeostática.
- Los eventos sinápticos en miniatura juegan un papel crítico en la regulación de la dinámica de la plasticidad sináptica homeostática.
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