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La potenciación a largo plazo depende de la liberación de D-serina de los astrocitos
Christian Henneberger1, Thomas Papouin, Stéphane H R Oliet
1UCL Institute of Neurology, University College London, London WC1N 3BG, UK.
Nature
|January 16, 2010
Resumen
Astroglia libera D-serina para permitir la potenciación a largo plazo (LTP) dependiente del receptor de N-metil-D-aspartato (NMDAR), un proceso clave para la memoria. Este estudio confirma que la D-serina derivada de los astrocitos es crucial para la plasticidad sináptica.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología celular Biología celular.
- La plasticidad sináptica.
Sus antecedentes:
- La potenciación a largo plazo (LTP) es un modelo para los mecanismos de memoria, clásicamente dependiente de los receptores de N-metil-D-aspartato (NMDAR).
- Se ha propuesto el papel de Astroglia en la regulación de la activación de NMDAR a través de la liberación de D-serina, pero sigue siendo controvertido debido a pruebas experimentales contradictorias.
- Se ha cuestionado la relevancia fisiológica de estudios previos sobre la participación glial en la LTP.
Objetivo del estudio:
- Investigar el papel directo de la señalización de calcio (Ca2+) de los astrocitos en el control de la LTP dependiente de NMDAR.
- Para determinar si la D-serina derivada de los astrocitos es esencial para la inducción de LTP en el área del hipocampo CA1.
Principales métodos:
- Apretando el Ca2+ interno en astrocitos CA1 individuales para observar los efectos en la sinapsis excitatoria cercana LTP.
- Invertir el bloqueo de la LTP utilizando D-serina o glicina exógena.
- El agotamiento de la D-serina o la interrupción de la exocitosis en astrocitos individuales para evaluar la LTP.
- Medición de la ocupación del sitio del co-agonista NMDAR.
Principales resultados:
- El apretamiento del Ca2+ interno en los astrocitos CA1 bloqueó la inducción de LTP en las sinapsis cercanas al reducir la ocupación del sitio del co-agonista NMDAR.
- Este bloqueo de la LTP fue reversible con D-serina o glicina exógenas.
- El agotamiento de la D-serina o la interrupción de la exocitosis en los astrocitos individuales también bloquearon la LTP local.
Conclusiones:
- La liberación de D-serina dependiente del Ca2+ de los astrocitos es un mecanismo crítico que controla la plasticidad sináptica dependiente del NMDAR.
- Este mecanismo regula la LTP a través de un gran número de sinapsis excitatorias en las cercanías del astrocito.
- Los hallazgos resuelven la controversia en torno a la participación de la glia en la inducción de la LTP.
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