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Demonstrates riluzole's effect on BK Ca channel activity in neuroendocrine cells, suggesting its regulatory role.
Background Riluzole is known to be an inhibitor of glutamatergic neurotransmission. Transmitter release from nerve terminals can be regulated by the activity of large-conductance Ca 2+ -activated K + (BK Ca ) channels. Methods The ionic mechanism of actions of riluzole was investigated in neuroendocrine (GH 3 and PC12 cells), using the whole-cell patch-clamp and inside-out excised patch configurations. Results In GH 3 cells, riluzole at 0.3-100 µmol/L increased the amplitude of Ca 2+ -activated K + current (I K(Ca) ) in a concentration-dependent manner with a half maximal concentration of 5 µmol/L. The riluzole-induced increase in outward current was not be suppressed by glibenclamide (10 µmol/L) or apamin (200 nmol/L). However, iberiotoxin (200 nmol/L) or tetrandrine (10 µmol/L) can effectively suppress riluzole-induced I K(Ca) . Under inside-out patch recording mode, riluzole (10 µmol/L) applied intracellularly can increase the opening probability of large-conductance Ca 2+ -activated K + (BK Ca ) channels, but did not affect their single-channel conductance. The riluzole-induced change in the kinetic behavior of BK Ca channels is due to an increase in mean open time and a decrease in mean closed time. Riluzole caused a left shift in the midpoint for voltage-dependent opening. Riluzole-stimulated activity of BK Ca is independent on internal Ca 2+ . Riluzole (30 µmol/L) did not affect the amplitude of voltage-dependent K + current, but it produced a slight reduction of L-type voltage-dependent Ca 2+ current. Under current clamp mode, riluzole (10 µmol/L) decreased the firing rate of action potentials induced by thyrotropin releasing hormone (10 µmol/L) in GH 3 cells. In rat pheochromocytoma PC12 cells, riluzole also increased the activity of BK Ca channels without altering their channel conductance. Conclusion This study shows that riluzole can stimulate the activity of BK Ca channel in neuroendocrine cells.
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Wu et al. (1999) studied this question.
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