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El PRG-1 sináptico modula la transmisión excitatoria a través de la señalización mediada por fosfato lipídico
Thorsten Trimbuch1, Prateep Beed, Johannes Vogt
1Institute of Cell Biology and Neurobiology and NeuroCure, Charité, Universitätsmedizin Berlin, Berlin, Germany.
Cell
|September 22, 2009
Resumen
El gen 1 relacionado con la plasticidad (PRG-1) regula la excitabilidad del hipocampo al interactuar con los receptores del ácido lisofosfatídico (LPA). Su ausencia causa convulsiones, pero restaurar PRG-1 o bloquear la señalización de LPA previene esta hiperexcitabilidad.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- El gen-1 relacionado con la plasticidad (PRG-1) es una proteína de membrana específica del cerebro.
- PRG-1 está asociado con las fosfatasas de fosfato lipídico y funciona en las sinapsis excitatorias en el hipocampo.
- La deficiencia de PRG-1 en ratones resulta en ataques epilépticos y potenciales postsinápticos excitatorios mejorados (EPSC).
Objetivo del estudio:
- Para investigar el papel de PRG-1 en la modulación de la excitación sináptica.
- Para determinar la participación del ácido lisofosfatídico (LPA) y su receptor en la función de PRG-1.
- Para aclarar el mecanismo por el cual PRG-1 controla la excitabilidad del hipocampo.
Principales métodos:
- In utero electroporación de PRG-1 en ratones con deficiencia.
- Mutagénesis dirigida al sitio del dominio extracelular PRG-1.
- Aplicación in vitro de LPA a ratones de tipo salvaje y ratones con deficiencia de receptores de LPA (2).
- Evaluación de la absorción de fosfolípidos en las neuronas con deficiencia de PRG-1.
- Análisis de ratones con deficiencia de los receptores PRG-1/LPA2).
Principales resultados:
- PRG-1 modula la excitación en la unión sináptica.
- La mutación del dominio extracelular PRG-1, crucial para la interacción de LPA, abolió su efecto antiepiléptico.
- La aplicación de LPA indujo hiperexcitabilidad en animales de tipo salvaje pero no con deficiencia de receptores de LPA.
- La absorción de fosfolípidos se redujo en las neuronas con deficiencia de PRG-1.
- La fisiopatología en ratones con deficiencia de PRG-1 se revirtió en animales con deficiencia de los receptores PRG-1/LPA (2).
Conclusiones:
- PRG-1 juega un papel crítico en la regulación de la excitabilidad del hipocampo.
- La función de PRG-1 depende de su interacción con los receptores presinápticos de LPA.
- PRG-1 actúa como un modulador clave de la transmisión sináptica a través de la señalización de los receptores LPA.
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