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Salud Mental 2007; 30 (2)
Idioma: Español
Referencias bibliográficas: 63
Paginas: 11-18
Archivo PDF: 69.97 Kb.
RESUMEN
Una de las características de los circuitos neuronales es que sus componentes, las neuronas, pueden presentar actividad eléctrica sincrónica y, gracias a ésta, generar actividad oscilatoria. Esta actividad se ha asociado a diversas funciones fisiológicas como el procesamiento de información sensorial, la memoria, el ciclo vigiliasueño y la conciencia. La actividad oscilatoria de un circuito neuronal está mediada por i) las propiedades intrínsecas de sus células, ii) la arquitectura de sus conexiones y iii) la dinámica de sus interacciones sinápticas. A nivel celular, las señales sinápticas pueden generar oscilaciones subumbrales del potencial de membrana y regular la frecuencia de disparo. Estas oscilaciones modulan la respuesta celular a las entradas sinápticas que ocurren en frecuencias funcionalmente relevantes y que, finalmente, producen los diferentes ritmos cerebrales.
A nivel estructural, el conjunto de proyecciones axonales de corto, mediano y largo alcance, permiten que módulos discretos, pero interconectados, oscilen en sincronía a lo largo de amplias regiones cerebrales.
En esta revisión, resaltamos la importancia que tienen las interacciones sinápticas, excitadora e inhibidora, en la regulación y mantenimiento de la sincronía del disparo en grupos neuronales. Abordamos también el impacto de la plasticidad de corto y largo plazo de la transmisión GABAérgica en la modulación de las propiedades sinápticas, las oscilaciones neuronales y su participación en la generación de ritmos hiper-sincrónicos, asociados con las descargas epilépticas y las alteraciones que éstas últimas producen en los mecanismos de inhibición sináptica. Por ejemplo, después de una crisis convulsiva generalizada o de inducir un estado de hiperexcitación, las células granulares glutamatérgicas del giro dentado del hipocampo, presentan modificaciones que les permiten sintetizar y liberar GABA, que actúa sobre receptores pre- y postsinápticos.
En este escenario, el GABA liberado espontáneamente de las células granulares, inhibe las oscilaciones de ~20 Hz en la zona CA3 del hipocampo. Se ha propuesto que este mecanismo, activado por crisis convulsivas, podría servir para limitar la actividad de la red neuronal en respuesta a incrementos de excitabilidad. De igual forma, su presencia se ha asociado con los efectos deletéreos que tienen las crisis convulsivas sobre el aprendizaje y la consolidación de memoria, particularmente durante la fase post-ictal. Finalmente discutimos el posible papel computacional que las oscilaciones neuronales tienen en la representación de información sensorial.
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