The K conductance (gK) kinetics were studied in voltage-clamped frog nodes (Rana ridibunda) in double-pulse experiments. The Cole-Moore translation for gK--t curves associated with different initial potentials (E) was only observed with a small percentage of fibers. The absence of the translation was found to be caused by the involvement of an additional, slow, gK component. This component cannot be attributed to a multiple-state performance of the k channel. It can only be accounted for by a separate, slow K channel, the fast channel being the same as the n4 K channel in R. pipiens. The slow K channel is characterized by weaker sensitivity to TEA, smaller density, weaker potential (E) dependence, and somewhat more negative E range of activation than the fast K channel. According to characteristics of the slow K system, three types of fibers were found. In Type I fibers (most numerous) the slow K channel behaves as and n4 HH channel. In Type II fibers (the second largest group found) the slow K channel obeys the HH kinetics within a certain E range only; beyond this range the exponential decline of the slow gK component is preceded by an E-dependent delay, its kinetics after the delay being the same as those in Type I fibers. In Type III fibers (rare) the slow K channel is lacking, and it is only in these fibers that the Cole-Moore translation of the measured gK--t curves can be observed directly. The physiological role of the fast and slow K channel in amphibian nerves is briefly discussed.

In experiments on rat pups we studied the effect of clonidine on potential-dependent Na+ currents in dorsal root ganglia by the voltage clamp method. Clonidine decreased the amplitude of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium currents. The range of acting concentrations and the absence of modulatory effect of norepinephrine on the efficiency of clonidine-induced blockade of sodium currents suggest that this blockade results from a direct interaction of clonidine with sodium channels.

The functioning of the electromechanical connection during tetanic contraction in frog skeletal muscle was studied. Analysis using caffeine, calcium-free medium, the ryanodine receptor blocker dantrolene, and the Ca-ATPase inhibitor thapsigargin showed that the initial increase in tetanus, as in twitch contractions, did not require the presence of calcium ions in the surrounding medium, which is in agreement with published data. Contraction was accompanied by activation of potential-dependent release of calcium from the sarcoplasmic reticulum. In contrast, the secondary rise phase and/or the duration of the tetanus plateau were critically dependent on the present of Ca2+ in the surrounding medium. Given that contraction in this situation was inhibited by dantrolene, activation of prolonged contraction was also mediated by calcium released from the sarcoplasmic reticulum, though ryanodine receptors were now activated not by changes in the membrane potential but by the influx of external calcium. Thus, external calcium plays a significant role in the formation of prolonged contractile responses, providing for longer-lasting maintenance of power in contracted muscles.

The effects of ethanol on tetrodotoxin-sensitive (TTXs) and tetrodotoxin-resistant (TTXr) sodium channels in rat spinal ganglia were studied using a patch-clamp method. Application of ethanol (10 and 100 mM) to both sides of membranes resulted in decreases in the reversion potentials of both types of sodium channels. In the case of TTXr channels, ethanol decreased their selectivity in relation to Na ions and altered the sequence of ion selectivity of these channels for different cations from row X to row XI of the Eisenman selectivity classification. It is suggested that this change in ion selectivity is associated with ethanol-induced disruption of hydrogen bonds which stabilize the spatial structure of ion channel macromolecules, which may lead to changes in the steric parameters of the pores formed by these channels.