ABSTRACT
The opiate analgetic promedol and non-opiate analgetics analgin, clonidine, baclofen, tolibut, vasopressin and calcitonin given in adequate doses block the inward electrosensitive sodium transmembrane ionic current of neurons. Like some drugs which do not exhibit any analgetic effect, promedol, analgin, clonidine, vasopressin and calcitonin also block the electrosensitive delayed potassium current. It is assumed that the blocking of the sodium ionic current may be one of the potential analgetic mechanisms at the neuronal level.
Subject(s)
Analgesics, Opioid/pharmacology , Analgesics/pharmacology , Neurons/drug effects , Animals , Cell Membrane/drug effects , Cell Membrane/physiology , Electric Stimulation , Electrophysiology , In Vitro Techniques , Lymnaea , Neurons/physiology , Potassium Channels/drug effects , Potassium Channels/physiology , Sodium Channels/drug effects , Sodium Channels/physiologyABSTRACT
It is shown in this work that vasopressin at the concentrations of 1 x 10(-16) to 1 x 10(-6) mol/l decreased statistically significant the amplitude of the electrosensitive sodium and calcium ionic currents of the mollusc's Lymnaea stagnalis neuronal membrane. This peptide increased the amplitude of the fast potassium current at the concentration of 1 x 10(-16) and 1 x 10(-15) mol/l. It decreased the fast potassium current and did not change the slow potassium current at the concentrations more than 1 x 10(-9) mol/l.
Subject(s)
Arginine Vasopressin/pharmacology , Neurons/drug effects , Animals , Cell Membrane/drug effects , Cell Membrane/physiology , Dose-Response Relationship, Drug , In Vitro Techniques , Membrane Potentials/drug effects , Membrane Potentials/physiology , Neurons/physiology , Potassium Channels/drug effects , Potassium Channels/physiology , Snails , Sodium Channels/drug effects , Sodium Channels/physiologySubject(s)
Mollusca/drug effects , Neurons/drug effects , Neuropeptides/pharmacology , gamma-Aminobutyric Acid/pharmacology , Action Potentials/drug effects , Adrenocorticotropic Hormone/pharmacology , Animals , Cell Membrane/drug effects , Cell Membrane/physiology , Delta Sleep-Inducing Peptide/analogs & derivatives , Delta Sleep-Inducing Peptide/pharmacology , Dose-Response Relationship, Drug , Drug Interactions , Membrane Potentials/drug effects , Neurons/physiologyABSTRACT
Chlorcholine chloride (CCC) the molecule of which has no other group, characteristic of acetylcholine (Ach), causes an effective cholinomimetic action on the surface membrane of the mollusc neurons A and B. As the concentration of Ach and CCC increases from 10(-6) to 10(-3) M the resting potential (RP) and the membrane resistance (R) of the neuron A first increases then decreases. The increase of Ach and CCC concentration causes in the neuron B only a decrease of the above mentioned parameters. The data point to the necessity of improving the ideas about the structure of cholinoreceptors and mechanism of cholinoreceptor-cholinomimetic interaction.
Subject(s)
Acetylcholine/pharmacology , Choline/analogs & derivatives , Membrane Potentials/drug effects , Mollusca/cytology , Neurons/drug effects , Animals , Electric Conductivity , Receptors, Cholinergic/drug effectsABSTRACT
Activation of the electrogenic sodium pump by means of increasing concentration of intracellular sodium ions in identified neurons A and B of the mollusc was followed by the hyperpolarization, decrease of the excitability, and depression of the neurons rhythmic activity. Apart from that, the amplitude and the maximal rates of rise of ascending (VB) and descending (VH) phases of action potential (AP) were almost unchanged. The depression of the electrogenic sodium pump activity due to 2,4-DNP and potassium-free medium, led to the depolarization, increase of excitability and frequency of the rhythmic activity, and decrease of AP, VB, and VH. The decrease and increase of the excitability may be explained by the changes of the critical level of depolarization. The decrease of AP, VB and VH may be accounted for by the changes of time parameters of activation and inactivation of sodium and potassium channels which are characteristic for the depolarization effect.
Subject(s)
Membrane Potentials , Mollusca/physiology , Neurons/physiology , Sodium/physiology , Action Potentials/drug effects , Animals , Biological Transport, Active , Dinitrophenols/pharmacology , Membrane Potentials/drug effectsABSTRACT
Action potentials (AP) of neurons A and B could be only elicited in the presence of Na-+ ions. An increase in [Ca-++]0 led to depolarization of neurons, enhancement of their excitability, AP, overshoot, of positive afterpotential, AP duration, AP maximal rate of fall (Vf) and to decrease in AP maximal rate of rise (Vr). After addition of CaCl2 up to 50 mmoles into the Ringer solution, the membrane resistance (R) increased. If the [Na-+]0 was equimolarly diminished, R increased up to the [Ca-++]0 30 mmoles, but at greater [Ca-++]0 R fall below the initial value. The regularities were independent of the initial value of resting potential (RP). At high [Ca-++]0 Ca-++ contributed to the generation of the inward current during AP while Na-+ caused an increase in ionic (calcium) membrane permeability at rest. At high [Ca-++]0, Na-+ was also necessary for support of membrane channels which maintained the inward and outward currents during the AP.