Accelerating effects of pentobarbitone on the inactivation process of the calcium current in Helix neurones

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Abstract
The effect of pentobarbitone on Ca2+ current (ICa), separated from other ionic currents was studied under voltage clamp using a suction pipette technique in Helix neurones. Pentobarbitone depressed the maximal peak amplitude (MPA) of ICa in a concentration‐dependent manner without shifting the current‐voltage (I‐V) relationships along the voltage axis. Increases in external Ca2+‐concentration ([Ca2+]***o) overcame the inhibitory action of the agent on MPA. Pentobarbitone markedly accelerated the decay phase of ICa which took a distinctly different time course from that of the control. The accelerating action of the agent on the decay phase of ICa was not overcome by increases in [Ca2+]o. In the presence of internal EGTA (20 mm), pentobarbitone also accelerated the decay of ICa. Changes in pH of the external perfusing solution altered the potency of pentobarbitone in depressing MPA; in the presence of pentobarbitone (3 × 10−4 m) at pH of 7.0, 8.0 and 9.0, fractional inhibition was approx. 46%, 21% and 4%, respectively. Internal application of pentobarbitone (10−4‐10−3 m) inhibited MPA, but exerted no effect on the decay phase of ICa. Pentobarbitone (10−4 m) markedly accelerated the decrease of MPA of ICa induced by repetitive stimuli applied at an interval of 150 ms, indicating a use‐dependent depression of MPA. Results provide evidence that pentobarbitone has a dual action on ICa, inhibiting MPA and accelerating the decay phase of ICa.