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Interleukin-1β inhibits the amplitudes of voltage-gated Na(+) currents and action potential in cultured cortical neurons of rat / 生理学报
Acta Physiologica Sinica ; (6): 131-137, 2011.
Artículo en Chino | WPRIM | ID: wpr-337694
ABSTRACT
Interleukin-1β (IL-1β) is an important proinflammatory cytokine and plays key roles in physiological and pathophysiological processes of central nervous system (CNS). The voltage-gated Na(+) channels are essential for electrical properties of excitable cells and control the excitability and action potential (AP) of neurons. Recent studies have showed the relationship between IL-1β and voltage-gated channels. In this work, cultured cortical neurons of rat were treated by 10 ng/mL of IL-1β for 24 h, and then voltage-gated Na(+) currents were recorded using voltage-clamp technique. The results indicated that IL-1β reduced the amplitude of Na(+) currents without any changes in activation or inactivation properties. The current-clamp recording showed that IL-1β reduced the amplitude of AP but not the threshold. These data indicate that IL-1β inhibits the voltage-gated Na(+) currents and the amplitude of AP, and suggest that essential roles of voltage-gated Na(+) channels may be changed by IL-1β. New information about effects of IL-1β on injuries and diseases of CNS was provided.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Fisiología / Potenciales de Acción / Células Cultivadas / Corteza Cerebral / Ratas Sprague-Dawley / Biología Celular / Interleucina-1beta / Canales de Sodio Activados por Voltaje / Neuronas Límite: Animales Idioma: Chino Revista: Acta Physiologica Sinica Año: 2011 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Fisiología / Potenciales de Acción / Células Cultivadas / Corteza Cerebral / Ratas Sprague-Dawley / Biología Celular / Interleucina-1beta / Canales de Sodio Activados por Voltaje / Neuronas Límite: Animales Idioma: Chino Revista: Acta Physiologica Sinica Año: 2011 Tipo del documento: Artículo