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Published on: July 17, 2011
La liberación de GABA tónico mediado por canales desde la glia
Soojung Lee1, Bo-Eun Yoon, Ken Berglund
1Center for Neural Science, Korea Institute of Science and Technology (KIST), Seoul, Korea.
Science (New York, N.Y.)
|October 9, 2010
Resumen
Las células gliales liberan el neurotransmisor inhibidor ácido gamma-aminobutírico (GABA) a través del canal Bestrophin 1 (Best1), mediando la inhibición tónica en el cerebelo. Este descubrimiento revela un nuevo mecanismo para la comunicación neuronal glial en la inhibición sináptica.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología celular Biología celular.
- La neuroquímica es la neuroquímica.
Sus antecedentes:
- La inhibición sináptica se basa tanto en la liberación tónica como en la fase del ácido gamma-aminobutírico (GABA).
- El mecanismo preciso que rige la liberación tónica de GABA sigue siendo en gran medida indeterminado.
- Se entiende que la liberación de GABA en fase se origina en la exocitosis neuronal dependiente de Ca(2+).
Objetivo del estudio:
- Para dilucidar el mecanismo molecular subyacente a la liberación tónica de GABA en el cerebelo.
- Para investigar el papel de las células gliales y canales iónicos específicos en la inhibición tónica.
- Para establecer la contribución del GABA derivado del glial a la función neuronal.
Principales métodos:
- Utilizó grabaciones electrofisiológicas para evaluar la inhibición sináptica.
- Se emplearon técnicas de silenciamiento genético para investigar el papel de la Bestrofina 1 (Best1).
- Realizó la expresión selectiva de Best1 en las células gliales para rescatar la inhibición tónica.
Principales resultados:
- Identificó la permeación de GABA a través del canal aniónico Bestrophin 1 (Best1) como la fuente de la liberación tónica de GABA de las células gliales.
- Se demostró que el silenciamiento de Best1 elimina por completo la inhibición tónica en el cerebelo.
- Se demostró que la reexpresión selectiva de Best1 en las células gliales restaura completamente la inhibición tónica.
Conclusiones:
- Establecido Bestrophin 1 (Best1) como el jugador molecular clave que media la liberación tónica de GABA de las células gliales.
- Se identificó una nueva vía para la comunicación glio-neuronal en la regulación de la inhibición sináptica.
- Destacó el papel crítico de las células gliales en la inhibición tónica a través de la permeación de GABA mediada por Best1.
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