[The role of intracellular processes in regulating neuronal sensitivity to acetylcholine]. / Rol' vnutrikletochnykh protsessov v reguliatsii chuvstvitel'nosti neironov k atsetilkholinu.

Intracellular regulatory mechanisms of neuronal response to acetylcholine were studied on intracellularly perfused isolated neurones of Lymnaea stagnalis using voltage-clamp technique. It was found that at the change of concentration of free intracellular Ca2+ from 0.06 to 0.7 microM the inhibitory effect of intracellularly added serotonin depends on Ca2+, and the modulation of acetylcholine responses by intracellular serotonin is unchanged. The blockers of calmoduline trifluoperazine and W-7 inhibit inward acetylcholine current at both intra- and extracellular introduction. Possible mechanisms mediating the effect of intracellularly added serotonin on the membrane cholinoreceptors of neurones are discussed.

[Mechanisms of the interaction of neurotransmitter systems]. / Mekhanizmy vzaimodeistviia neirotransmitternykh sistem.

Interaction between different neurotransmitter systems has been revealed on various objects--the myocardium, identified, intact and internally perfused isolated neurons of molluscs. In frog myocardium, the inhibitory effect of adrenaline on cholinergic response may be simulated by theophylline and cholera toxin, i.e. the substances which indirectly increase intracellular content of cAMP. Another interaction reaction--inhibition of the response to adrenaline by acetylcholine--may be reproduced by imidazole, which decreases cAMP content due to activation of phosphodiesterase. Two types of interaction between serotonin and acetylcholine were revealed in the identified neurons of the snail Helix pomatia. In some of the neurons, serotonin increases acetylcholine depolarization, whereas in other ones decreases the latter. Both the increase and the decrease of responses to acetylcholine may be reproduced by theophylline. On intracellularly perfused neurons of Lymnaea stagnalis, modulation of acetylcholine responses of cell by biogenic amines was observed, the effect being induced by the drugs added not only to the surface membrane, but to intracellular medium as well.

[Changes in the acetylcholine responses of perfused neurons of Limnaea stagnalis during internal and external exposure of the cell]. / Izmenenie atsetilkholinovykh otvetov perfuziruemykh neironov prudovika pri deistvii serotonina snaruzhi i iznutri kletki.

The modifying effect of extra- and intracellular administration of serotonin on inward currents generated by the cell at extracellular application of acetylcholine was studied. The study was made on nonidentified isolated neurons of the fresh water mollusc Lymnaea stagnalis using the voltage-clamp and intracellular perfusion methods. In roughly a half of the studied cells serotonin being added intra- and extracellularly produced a decrease in the response to acetylcholine. In the other half of neurons serotonin being added intracellularly increased the acetylcholine response, but applied extracellularly showed the opposite effect: it decreased the magnitude of inward acetylcholine currents. The blocker of serotonin receptors, cyproheptadine, blocks the enhancing effect of serotonin on the intracellular addition of the mediator, but mimics the inhibitory effect of serotonin on acetylcholine response. The data obtained on the neurons of molluscs suggest the existence of intracellular receptors of serotonin one whose possible functions is the regulation of sensitivity of the cell surface cholinoreceptors.

[2 Phases of the inotropic action of adrenaline. Calcium dependence]. / Dve fazy inotropnogo deistviia adrenalina. Kal'tsievaia zavisimost'.

The biphasic inotropic effect of adrenaline administered for a long time (30 min) was studied on a frog ventricular strip. The fall in the contraction amplitude got more pronounced as the intensity of Ca ions entrance into the myocardial cells was potentiated by the increased frequency of stimulation and calcium or adrenaline concentrations were raised. The mechanisms of the adrenaline-induced decrease in the contraction amplitude are discussed.

[Effect of cadmium on electromechanical coupling in the frog myocardium]. / Vliianie ionov kadmiia na élektromekhanicheskoe sopriazhenie v miokarde liagushki.

CdCl2 (0.2-0.5 mM) shortened the duration of action potential and reduced the tension of frog ventricular strips. CdCl2 completely blocked slow AP in partially depolarized strips and abolished both the tonic and phasic components of KCl-induced contractures. CdCl2 prevents adrenaline, NiCl2 and low-Na Ringer solution to produce tension potentiation. Cd seems to block the slow Na-Ca channels of frog myocardium and disturb intracellular Ca distribution by its ability to block protein SH-groups.

[Effect of catecholamines on the electrical and mechanical activity of frog myocardium after increasing the duration of action potentials with nickel ions]. / Vliianie katekholaminov na élektricheskuiu i mekhanicheskuiu aktivnosti miokarda liagushki v usloviiakh uvelicheniia dlitel'nosti potentsialov deistviia ionami nikelia.

The "chemical current--clump" method revealed that, after nickel ions (0.5 mM) had produced prolongation of AP, catecholamines (CA) increased the force and shortened the relaxation phase of isometric tension in the frog ventricular myocardium. Additional blockade of Ca++--channels with 2 mM NiCl2 or niphedipin inversed the positive inotropic effect of CA. Prevention of the ability of CA to increase the Ca--current and AP--duration unmasks the action of CA on intracellular stores.

[Study of the molecular structure and mechanisms of pond snail neuron cholinoreceptor function by means of in vivo chemical modification]. / Issledovanie molekuliarnoi struktury i mekhanizmov funktsionirovaniia kholinoretseptorov neironov prudovika s pomoshch'iu prizhiznennoi khimicheskoi modifikatsii.

The molecular structure of acetylcholine receptors (AChR) of Lymnaea stagnalis neurons has been studied using specific agents to definite chemical groups. The disulphide bond important for AChR function was discovered, the reduction of which by dithiotreitol (DTT) inactivates AChR. The drugs exciting AChR protect the disulphide bond against modification with DTT likely due to the conformational changes of an active site and its environment. Desensitized AChR can also be modified by DDT (if it is not occupied by agonist). It is suggested that the system transmitting the conformational change from the AChR active site to its ionophore is responsible for desensitization.