Abstract
The effects of ethanol (EtOH) on the early potassium current, IA, were examined in 3 identified neurons of Aplysia using voltage-clamp techniques. The primary effect of EtOH on this current was a pronounced increase in the time constant of decay. However, this effect was cell specific, being evident in cells MCC and R15 but not in cell B1. Other parameters of IA were not greatly affected in any of the cells, in comparison with the effects on decay time constant. Baseline parameters of IA were measured in each of the cells to determine whether subpopulations of IA channel might exist, and be differentially sensitive to EtOH. While differences did appear among cells, they were not consistent with an explanation of EtOH's actions based upon distribution of channel subtypes. The effect of EtOH on IA decay was dependent upon the voltage-clamp protocol used. When inactivation of IA developed at -20 mV, the slower development of inactivation noted above occurred. When inactivation without channel opening was produced by means of a prepulse to -40 mV, EtOH speeded up the development of inactivation. A number of possible explanations for these findings are discussed. Most of the effects of EtOH occurred within 1 min of application of the drug, suggesting relatively rapid access to the site of action. Effects continued to develop over succeeding minutes. This slower-developing effect may reflect either a delayed access to channels due to slower diffusion into or lateral movement within the lipid phase of the membrane, or it may indicate that channels are accessible to the EtOH molecule only when in certain states.
