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Published on: June 26, 2013
Los opioides bloquean la potenciación a largo plazo de las sinapsis inhibidoras
Fereshteh S Nugent1, Esther C Penick, Julie A Kauer
1Brown University, Department of Molecular Pharmacology, Physiology and Biotechnology, Providence, Rhode Island 02912, USA.
Nature
|April 27, 2007
Resumen
Los investigadores descubrieron una nueva forma de plasticidad sináptica en el cerebro.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- La plasticidad sináptica.
- Neurofarmacología y Neurofarmacología.
Sus antecedentes:
- La plasticidad sináptica, cambios en la fuerza sináptica, subyace al aprendizaje y la adicción.
- La plasticidad de las sinapsis inhibidoras que liberan GABA (ácido gamma-aminobutírico) se entiende menos.
- El área tegmental ventral es crucial para el desarrollo de la adicción a las drogas.
Objetivo del estudio:
- Para investigar la potenciación a largo plazo de la transmisión sináptica mediada por GABA (LTP) en las neuronas dopaminérgicas.
- Explorar los mecanismos subyacentes a esta nueva forma de plasticidad sináptica.
- Para examinar los efectos de la morfina en la LTP (GABA).
Principales métodos:
- Registros electrofisiológicos en rebanadas de cerebro de rata.
- Investigó la plasticidad heterosináptica que requiere la activación del receptor NMDA.
- Utilizó óxido nítrico como una molécula de señalización retrógrada.
Principales resultados:
- Identificó LTP ((GABA) en las neuronas de dopamina en el área tegmental ventral.
- Se ha demostrado que el LTP (GABA) es heterosináptico, mediado por el óxido nítrico inducido por el receptor NMDA.
- Se demostró que la exposición a la morfina, tanto in vitro como in vivo, previene la LTP (GABA).
Conclusiones:
- Las neuroadaptaciones inducidas por opioides en LTP (GABA) pueden contribuir a la adicción.
- El nuevo mecanismo implica la transmisión de señales de óxido nítrico desde las neuronas dopaminérgicas a los terminales GABA.
- Las estrategias terapéuticas dirigidas a los receptores GABA (A) pueden ser beneficiosas.
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