[Effect of several m-cholinoblockaders on the functioning of sodium potential-dependent channels of neuroblastoma cells]. / Vliianie nekotorykh m-kholinoblokatorov na funktsionirovanie natrievykh potentsialzavisimykh kanalov kletok neiroblastomy.

Effects of two central antimuscarinic drugs, namely N-methyl-4-piperidinol benzylate and tropine phenylcyclopentylglycolate on Na currents in internally dialyzed mouse neuroblastoma cells were studied using the suction-pipette voltage-clamp technique. Like amine local anesthetics, the both compounds produce two phenomenologically different types of sodium current inhibition: a steady block without conditioning and a cumulative (use-dependent) block which develops during repetitive membrane pulsing. The ability of these m-cholinoblockers to modulate voltage-dependent ionic permeability of the neuronal membranes is supposed to be one of possible components in the mechanism of their both main and accessory (non-synaptic) effects.

[Acetylcholinesterase expression and changes in the electrical excitability of neuroblastoma cells during their morphological differentiation induced by an increase in the pH of the medium]. / Ekspressiia atsetilkholinésterazy i izmeneniia élektrovozbudimosti v kletkakh neiroblastomy v khode ikh morfologicheskoi differentsirovki, indutsirovannoi povysheniem pH sredy.

Inhibition of cell division and outgrowth of neurites with average rate of 31.5 +/- 4.4 micrometers per hour were observed in neuroblastoma cultures of the Neuro 2a clonal line 24 hours after the increase in the culture medium pH from 7.4 to 8.2. The total neurite length per one cell was about 298 +/- 36 micron in average by the 9-10th days of treatment. Simultaneously, a gradual enhancement of acetylcholinesterase cytochemical appearance took place attaining its maximum level by the same time. The peak sodium conductance, taken as a measure of sodium tetrodotoxin-sensitive potential-dependent channel density, was the same both in nondifferentiated cells grown in suspension or monolayer cultures, and in morphologically differentiated ones. The data lead to a conclusion that biochemical (acetylcholinesterase probe) and electrophysiological (sodium channel density) signs can express independently of morphological differentiation.

[Effect of ruthenium red on the sodium channel inactivation of neuroblastoma cells]. / Vliianie rutenievogo krasnogo na inaktivatsiiu natrievykh kanalov kletok neiroblastomy.

Currents through sodium channels in the neuroblastoma cell membrane were measured after internal and external application of the ruthenium red. The treatment of the membrane by the dye resulted in a slowdown of inactivation kinetics of sodium currents and in the changes of activation and inactivation stationary parameters, which were more pronounced after internal application of the ruthenium red.

[Action of chloramine-T on the processes of sodium channel activation and inactivation in neuroblastoma cells]. / Issledovanie deistviia khloramina-T na protsessy aktivatsii i inaktivatsii natrievykh kanalov kletok neiroblastomy.

Effect of chloramine-T, the specific reagent on methionine residues, on gating of sodium channels was studied in neuroblastoma cell membrane. After the chloramine treatment the inactivation became slower, incomplete and the steepness of its voltage dependence considerably decreased; the inactivation curve was shifted towards depolarization. Time course of activation did not change. The activation curve shifted towards negative potentials, its slope being insignificantly decreased. Effective charge of activation as determined from the limiting logarithmic slope of the activation decreased by a factor of 1.17. Possible explanations of the phenomena observed are discussed.

Gating and selectivity of aconitine-modified sodium channels in neuroblastoma cells.

Currents through normal and aconitine-modified sodium channels in perfused neuroblastoma cells were measured under voltage-clamp conditions. Aconitine is shown to induce changes in channel selectivity so that channels become more permeable to NH4+ than to Na+. Aconitine induces the shift of voltage dependence of channel activation toward more negative potentials by about 20 mV. Aconitine-modified channels inactivate practically completely with a time-course similar to that for normal channels. Aconitine is effective when applied to either side of the membrane. Steady-state characteristics of the gating machinery of aconitine-modified channels are discussed in terms of three-state model. According to the model, aconitine increases the probability of finding the channel in open state, which is reflected in negative shift of the voltage dependence of activation. The model predicts that the larger this shift, the higher is the level of steady-state sodium conductance. The comparison of respective properties of aconitine-modified channels in neuroblastoma cell and frog nerve confirms this prediction. Aconitine is assumed to reach its receptor through the lipophilic part of the membrane.

[Aconitine modification of cell membrane sodium channels of a neuroblastoma]. / Modifikatsiia natrievykh kanalov membrany kletok neiroblastomy akonitinom.

Currents through normal and aconitine-modified sodium channels in the perfused neuroblastoma cell are measured under voltage clamp conditions. Aconitine shifts the voltage range of activation of the sodium channels towards more negative potentials by about 20 mV, and changes the selectivity, so that channels become more permeable to NH4+ than to Na+ ions. The currents through aconitine--modified channels are inactivated almost completely like those through the normal ones. Aconitine is effective when applied to both sides of the cell membrane. Steady-state characteristics of gating are discussed in terms of the model assuming three main states of the gate machinery: closed, open and inactivated.