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Las reservas de calcio regulan la polaridad y la especificidad de entrada de la modificación sináptica.
M Nishiyama1, K Hong, K Mikoshiba
1Department of Biology, University of California at San Diego, La Jolla 92093-0357, USA.
Nature
|December 16, 2000
Resumen
La plasticidad sináptica inducida por la actividad, como la potenciación a largo plazo (LTP) o la depresión (LTD), depende del calcio postsináptico. La afluencia de calcio y la liberación de los depósitos internos regulan la polaridad y la especificidad de la modificación sináptica.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- La plasticidad sináptica.
- Biología Molecular Biología Molecular
Sus antecedentes:
- La modificación sináptica, incluida la potenciación a largo plazo (LTP) y la depresión a largo plazo (LTD), es crucial para el desarrollo del sistema nervioso y la plasticidad.
- Los cambios dependientes de la actividad en la eficacia sináptica son fundamentales para el aprendizaje y la memoria.
- Una pregunta clave es si estas modificaciones se limitan a las sinapsis activadas.
Objetivo del estudio:
- Investigar el papel de la afluencia postsináptica de calcio y las reservas internas de calcio en la regulación de la plasticidad sináptica.
- Para determinar la especificidad de entrada de la potenciación a largo plazo (LTP) y la inducción de la depresión a largo plazo (LTD).
- Aclarar los mecanismos subyacentes a la polaridad y la especificidad de las modificaciones sinápticas inducidas por la actividad.
Principales métodos:
- Registros electrofisiológicos en la región CA1 del hipocampo.
- Bloqueo farmacológico de los receptores NMDA (N-metil-D-aspartato) para modular la afluencia postsináptica de calcio.
- La inhibición de los receptores de ryanodina y los receptores de trifosfato de inositol (InsP3) para estudiar la liberación de calcio intracelular.
- Eliminación genética de los receptores InsP3 tipo 1.
Principales resultados:
- El bloqueo parcial de los receptores NMDA convirtió LTP en LTD e indujo LTD en las entradas heterosinápticas.
- La inducción de la LTD homo-sináptica requería receptores funcionales de ryanodina, mientras que la LTD heterosináptica requería receptores InsP3.
- El bloqueo de los receptores de ryanodina abolió la LTD homo-sináptica pero no la LTD heterosináptica.
- La deleción genética de los receptores InsP3 tipo 1 convirtió a LTD en LTP y eliminó a LTD heterosináptico.
Conclusiones:
- El calcio postsináptico, influenciado por la afluencia y liberación de los receptores de ryanodina e InsP3, dicta tanto la dirección (LTP / LTD) como la especificidad de las modificaciones sinápticas.
- La activación diferencial de las reservas intracelulares de calcio juega un papel crítico en la determinación de la plasticidad homosináptica versus la heterosináptica.
- Estos hallazgos revelan un mecanismo sofisticado que controla la plasticidad sináptica basada en la dinámica del calcio.
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