Impaired neuronal function induced by the immune mediator leukotriene B4

Inflammatory cerebral processes, mediated by immunologically active substances or invading of macrophages are frequently associated with neuronal dysfunction. This study describes the effects of leukotriene B4 on membrane potential, membrane resistance and potassium currents of cultured cortical neurons from the embryonic rat. Leukotriene B4 (1 microM) did not depolarize cortical neurons but induced a reversible reduction of voltage-dependent potassium outward currents (IK) in a subpopulation of these cells (35%). The results suggest that, in comparison to astrocytes, cortical neurons lack receptors for LTB4 or its intracellular activation pathway. Immune mediators, such as leukotrienes, may contribute to neuronal dysfunction during inflammatory diseases by affecting neuronal membrane currents.