Article date: October 1994
By: G. Erdemli, K. Krnjevic, in Volume 113, Issue 2, pages 411-418
Membrane effects of cromakalim (Crom; 50–300 μm) were examined in CA1 neurones recorded mainly by intracellular, single‐electrode voltage‐clamping in slices (from Sprague‐Dawley rats) kept in an interface chamber at 33°C.
In 14 cells held at − 63 ± 3.5 mV, in the presence of tetrodotoxin, kynurenic acid and (in most cases) bicuculline, bath applied Crom produced no consistent change in holding current (‐ 59 ± 66pA) or input conductance (GN) (‐ 3.9 ± 5.2%).
Overall there were no significant changes in instantaneous inward rectification or in Q‐current inward relaxations.
In 18 out of 22 cells, outward currents, evoked by 0.5 s pulses to voltages > − 50 and < − 20 mV, were depressed by Crom (by 42 ± 11%, for n = 22). Because this effect was consistently seen in Ca current‐blocking media, containing either Mn and low Ca, or Cd (and also carbachol), the K channels depressed by Crom were probably of the delayed rectifier (IDR) type.
The Crom‐control difference current (ICrom) obtained with slow depolarizing ramps, had a biphasic character, inward in the voltage (V) range > − 50 < − 20 mV (where outward currents are depressed by Crom) and tending outward for V ≥ − 20 mV.
In 10 out of 11 cells, Crom potentiated a D‐like, slowly‐inactivating outward current (by 88 ± 31%, for n = 11).
The effects of Crom and of 2 min periods of anoxia were compared in 12 cells: unlike anoxia, Crom produced no consistent increases in GN; the currents evoked in the same cells by anoxia differed significantly from those evoked by Crom (by 150 ± 60 pA); the directions of current changes induced by Crom and anoxia respectively were not significantly correlated. Crom strongly depressed anoxic outward currents (by 80 ± 12%, n = 4).
Some Crom‐induced effects (increases in D‐like current and the outward current elicited at V ≥ − 20 mV) were always reversed by tolbutamide (1 μm), but much less consistently by glibenclamide (10–30 μm).
In conclusion, the effects of Crom, recorded with intracellular electrodes in CA1 neurones in slices, show little resemblance to the effects of activation of ATP‐sensitive K channels.
Membrane effects of cromakalim (Crom; 50–300 μm) were examined in CA1 neurones recorded mainly by intracellular, single‐electrode voltage‐clamping in slices (from Sprague‐Dawley rats) kept in an interface chamber at 33°C.
In 14 cells held at − 63 ± 3.5 mV, in the presence of tetrodotoxin, kynurenic acid and (in most cases) bicuculline, bath applied Crom produced no consistent change in holding current (‐ 59 ± 66pA) or input conductance (GN) (‐ 3.9 ± 5.2%).
Overall there were no significant changes in instantaneous inward rectification or in Q‐current inward relaxations.
In 18 out of 22 cells, outward currents, evoked by 0.5 s pulses to voltages > − 50 and < − 20 mV, were depressed by Crom (by 42 ± 11%, for n = 22). Because this effect was consistently seen in Ca current‐blocking media, containing either Mn and low Ca, or Cd (and also carbachol), the K channels depressed by Crom were probably of the delayed rectifier (IDR) type.
The Crom‐control difference current (ICrom) obtained with slow depolarizing ramps, had a biphasic character, inward in the voltage (V) range > − 50 < − 20 mV (where outward currents are depressed by Crom) and tending outward for V ≥ − 20 mV.
In 10 out of 11 cells, Crom potentiated a D‐like, slowly‐inactivating outward current (by 88 ± 31%, for n = 11).
The effects of Crom and of 2 min periods of anoxia were compared in 12 cells: unlike anoxia, Crom produced no consistent increases in GN; the currents evoked in the same cells by anoxia differed significantly from those evoked by Crom (by 150 ± 60 pA); the directions of current changes induced by Crom and anoxia respectively were not significantly correlated. Crom strongly depressed anoxic outward currents (by 80 ± 12%, n = 4).
Some Crom‐induced effects (increases in D‐like current and the outward current elicited at V ≥ − 20 mV) were always reversed by tolbutamide (1 μm), but much less consistently by glibenclamide (10–30 μm).
In conclusion, the effects of Crom, recorded with intracellular electrodes in CA1 neurones in slices, show little resemblance to the effects of activation of ATP‐sensitive K channels.
DOI: 10.1111/j.1476-5381.1994.tb17004.x
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