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2013, Número 1

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Biotecnol Apl 2013; 30 (1)


Excitotoxicidad y muerte neuronal en la epilepsia

Lorigados L, Orozco S, Morales L, Estupiñán B, García I, Rocha L

Idioma: Español
Referencias bibliográficas: 95
Paginas: 1-8
Archivo PDF: 396.47 Kb.


RESUMEN

La epilepsia es una afección neurológica de evolución crónica, recurrente, casi siempre progresiva, que afecta del 1 al 2 % de la población mundial. Modelos experimentales y estudios de imágenes neurológicas de pacientes con este padecimiento muestran que las crisis recurrentes provocan estrés oxidativo, relacionado fundamentalmente con la excitabilidad neuronal. La estimulación excesiva de los receptores de glutamato induce neurotoxicidad, un proceso que se ha defi nido como excitotoxicidad. Se considera que este puede ser el principal mecanismo de muerte celular en numerosas afecciones del sistema nervioso central, incluida la epilepsia. Desde los años 70 se han estudiado con profundidad las vías de señalización, los mecanismos moleculares y los sitios de acción relacionados con la excitotoxicidad; aunque de forma muy limitada en las enfermedades del sistema nervioso central. En particular, deberán evaluarse con especial cuidado la función crucial de la muerte neuronal y los mecanismos que se potencian con la sobreactivación de los receptores de glutamato, principalmente los relativos a las enfermedades neurológicas, con el fi n de intervenir de manera oportuna para retardar el desarrollo de estas afecciones neurológicas. Se repasan las evidencias clínicas y experimentales sobre las alteraciones del sistema glutamatérgico, las vías de muerte celular, la activación de las caspasas y de la familia de genes Bcl-2 involucrados, como moduladores de la muerte celular en la epilepsia. Tales hallazgos sustentan que en la epilepsia farmacorresistente convergen procesos excitotóxicos y de muerte neuronal apoptótica y necrótica.


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