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Retigabine (D-23129) is a new anticonvulsant compound which acts as a K + channel opener in neuronal cells. The aim of the present study was to further characterize the retigabine induced K + current. In nerve growth factor treated PC12 cells and in rat cortical neurones the application of retigabine activated a K + current. In contrast, however, no K + current activation was observed in untreated PC12 and in glial cells which were cultivated together with the neuronal cells. To characterise the retigabine activated K + current, K + channel blockers were used. The retigabine induced current was not affected by 1 and 10 mM 4-aminopyridine (4AP). Ba 2 + 1 mM resulted in a reduction of 88.6 9 3.0% (n= 5); 10 mM abolished the current. Tetraetylamonium (TEA), 1 and 10 mM, reduced the current by 23.6 93.1 and 61.6 93.7%, respectively. To investigate the current/voltage (I/V) relation of the current initiated by retigabine (10 mM), cells were clamped to a holding potential of -80 mV and a ramp stimulation protocol ( -120 to + 60 mV in 5 s) was applied prior to and during application of retigabine. Subtraction of the two traces yielded the current induced by retigabine. A nearly linear rel

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Author

Chris Rundfeldt

Publisher

Elsevier Science; Elsevier ; Elsevier BV (ISSN 0920-1211)

Published

1999

Language

EN

Field

Medicine (Health Sciences)