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Analgesia e hiperalgesia por la modulación mediada por GABA de la corteza cerebral
Luc Jasmin1, Samuel D Rabkin, Alberto Granato
1Department of Neurological Surgery, University of California, San Francisco, San Francisco, California 94143-0452, USA. ucpain@itsa.ucsf.edu
Nature
|July 18, 2003
Resumen
Los cambios en la neurotransmisión de ácido gamma-aminobutírico (GABA) en la corteza agranular insular rostral (RAIC) pueden modular la percepción del dolor. La mejora del GABA en el RAIC conduce a la analgesia, mientras que la activación de receptores específicos de GABA causa hiperalgesia.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Investigación del dolor Investigación del dolor.
- Biología Molecular Biología Molecular
Sus antecedentes:
- La percepción del dolor está influenciada por el estado de ánimo, la atención y la cognición.
- La corteza cerebral juega un papel en la modulación del dolor, pero los mecanismos neuronales subyacentes son poco conocidos.
- La corteza agranular insular rostral (RAIC) se activa por estímulos dolorosos, y el ácido gamma-aminobutírico (GABA) inhibe la actividad neuronal allí.
Objetivo del estudio:
- Para investigar el papel de la neurotransmisión GABA en el RAIC en la modulación del dolor.
- Para determinar cómo la alteración de los niveles de GABA en el RAIC afecta el umbral del dolor.
- Para dilucidar las vías neuronales involucradas en la modulación del dolor cortical.
Principales métodos:
- Los experimentos se llevaron a cabo en ratas que se movían libremente.
- Los niveles de GABA en el RAIC se alteraron utilizando inhibidores de enzimas y transferencia de genes mediada por vectores virales.
- Se midió la actividad neuronal y los umbrales de dolor.
- Se realizó una activación selectiva de las neuronas RAIC portadoras de receptores GABA (((B)).
Principales resultados:
- La modulación de la neurotransmisión GABA en el RAIC alteró los umbrales de dolor, induciendo analgesia o hiperalgesia.
- El aumento de GABA en el RAIC aumentó la inhibición descendente de las neuronas nociceptivas espinales, produciendo analgesia duradera.
- La activación de las neuronas RAIC portadoras del receptor GABA (B) condujo a la hiperalgesia a través de proyecciones a la amígdala.
Conclusiones:
- Los mecanismos GABAérgicos dentro del RAIC son críticos para regular el dolor.
- La corteza cerebral, específicamente el RAIC, puede ejercer un control de arriba hacia abajo sobre el procesamiento del dolor al alterar el umbral del dolor.
- Estos hallazgos ofrecen información sobre nuevos objetivos terapéuticos para el manejo del dolor.
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