Some effects of short-chain phospholipids and n-alkanes on a transient potassium current (IA) in identified Helix neurons.

Many effects of short-chain phospholipids and n-alkanes on the squid axon sodium current (INa) are consistent with mechanisms involving changes in membrane thickness. Here, we suggest that the actions of short-chain phospholipids on an A-type potassium current (IA) in two-microelectrode voltage clamped Helix D1 and F77 neurons are incompatible with such simple mechanisms. Diheptanoyl phosphatidylcholine (diC7PC, 0.2 and 0.3 mM) caused substantial (58 and 79%), and in some cases partially reversible, increases in IA amplitude. These were correlated with hyperpolarizing shifts of up to -7 mV in the voltage dependence of current activation. The voltage dependence of steady-state inactivation was also moved in the hyperpolarizing direction. These effects are the opposite of those described for squid INa. 0.5 Saturated n-pentane and saturated n-hexane caused significant (-3 and -6 mV) hyperpolarizing shifts in the voltage dependence of IA inactivation, qualitatively consistent with their effects on squid INa, while the voltage dependence of activation was moved slightly to the left or unchanged. Hydrocarbons had variable effects on peak current amplitude, although saturated n-pentane produced a clear suppression. DiC7PC caused a 25% increase in the time constant of macroscopic IA inactivation (tau b) but 0.5 saturated n-pentane and saturated n-hexane reduced tau b by 40%. The effects of these agents on current-clamped cells were broadly consistent with their opposing actions on tau b--phospholipids tended to reduce excitability and n-alkanes tended to increase it. Possible mechanisms of IA perturbation are discussed.