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A S Pivovarov

Publications and source records attributed to A S Pivovarov.

At least 19 recordsLinked to original sources
PubMed2006

Methiothepin-sensitive serotonin receptors are involved in the postsynaptic mechanism of sensitization of the defensive response in the common snail.

Rhythmic electrical stimulation of the snail foot leads to sensitization of the defensive reflex. This sensitization has dynamics similar to those of posttetanic potentiation of the amplitude of the acetylcholine-evoked influx current of defensive behavior command neurons in the common snail. It is likely that an increase in the cholinosensitivity of the somatic membrane of defensive behavior command neurons in the common snail may be involved in the mechanism of sensitization of the animal's defensive response. Methiothepin, an antagonist of serotonin receptors, prevented the posttetanic potentiation of the acetylcholine-evoked influx current as well as behavioral sensitization. Serotonin, like methiothepin, also impaired posttetanic potentiation of the acetylcholine-evoked influx current. It is suggested that methiothepin-sensitive serotonin receptors are involved in the postsynaptic mechanism of behavioral sensitization.

Acetylcholine↗
PubMed2005

Inositol triphosphate and ryanodine receptors in the control of the cholinosensitivity of common snail neurons by the Na,K pump during habituation.

The effects of the Na,K pump inhibitor ouabain on habituation of the common snail to tactile stimulation were identical to the ouabain-induced modification of the decrease in the cholinosensitivity of defensive behavior command neurons in the common snail in a cellular model of habituation. Studies addressed the effects of intracellularly delivered ligands of two types of Ca2+ depot receptors--inositol triphosphate (IP3) receptors and ryanodine receptors--on the action of ouabain in the cellular analog of habituation. The IP3 receptor antagonist heparin (0.1 mM), the IP3 receptor agonist inositol triphosphate (0.1 mM), and the ryanodine-dependent Ca2+ mobilization inhibitor dantrolene (0.1 mM) prevented ouabain from modifying the depression of the evoked acetylcholine current. The ryanodine agonist/antagonist ryanodine was used at two concentrations (0.1 and 1 mM) and neither had any effect on the action of ouabain. It is concluded that Ca2+ mobilized from intracellular Ca2+ depots via IP3 receptors is involved in the neuronal mechanism of regulation of the habitation of the common snail to tactile stimulation by the Na,K pump.

Acetylcholine↗
PubMed2004

An apparatus for recording defensive responses to tactile stimulation in the ground snail.

We describe here an original working experimental apparatus for non-invasive objective recording of the magnitudes of defensive responses to tactile stimulation in the ground snail. The apparatus includes a tracking device that ensures that the snail's position relative to a light and photodiode remains constant as it ascends a cylinder rotating about a horizontal axis. The device providing tactile stimulation is based on a loudspeaker circuit and provides blows of dosed energy. The snail responds to the tactile stimulation by retracting the antennae, head, and foot, which decreases the area of its shadow; this is recorded by a photodiode.

Animals↗
PubMed2004

Relationship between post-tetanic potentiation of the cholinosensitivity of neurons in the common snail and a humoral factor.

Plots of post-tetanic changes in the amplitude of the acetylcholine-evoked influx current (the ACh current) in common snail command neurons were compared in different experimental conditions: with and without a flow of physiological saline through the chamber containing snail ganglia. Flow of physiological saline through the chamber containing the ganglia decreased the latent period and reduced the magnitude of the post-tetanic increase in the neuronal ACh current. The earlier and less marked post-tetanic potentiation of the ACh current in neurons with a flow of physiological saline through the chamber containing the ganglia are evidence for the involvement of a humoral factor in the mechanism of the post-tetanic increases in cholinosensitivity of the somatic membranes of postsynaptic neurons.

Acetylcholine↗
PubMed2003

Involvement of Na/Ca exchange and intracellular mobilized Ca2+ in Na,K-pump-mediated control of depression of the cholinosensitivy of common snail neurons [correction of neorons] using a cellular analog of habituation.

The role of Na/Ca exchange and intracellular mobilized Ca2+ in modifying the depression of defensive behavior command neuron cholinosensitivity induced by the the Na,K pump inhibitor ouabain was studied in common snails using a cellular analog of habituation. Integral transmembrane acetylcholine-evoked currents (ACh currents) were recorded using a two-electrode membrane potential clamping technique. Decreases in neuron cholinosensitivity in the cellular analog of habituation were assessed in terms of the depth of depression of the amplitude of ACh currents during rhythmic local application of acetylcholine (with interstimulus intervals of 2-4 min) to the somatic membrane. The Na/Ca exchange inhibitor benzamyl (applied extracellularly, 15-35 microM) and two specific endoplasmic reticulum Ca-ATPase inhibitors, cyclopiazonic acid and thapsigargin (applied intracellularly. 0.1 mM) prevented modification of depression of the ACh current by ouabain (100 microM). It is concluded that Na/Ca exchange and the release of mobilized Ca2+ from intracellular calcium depots are involved in the mechanism by which the Na,K pump controls the depression of neuron cholinosensitivity in the cellular analog of habituation.

Acetylcholine↗
PubMed2003

Modulatory serotonin receptors on the soma of command neurons in edible snail.

Local application of serotonin (5-hydroxytryptamine, 5-HT) to the soma of command neurons LPa2, LPa3, PPa3, and PPa2 of edible snail Helix lucorum reversibly decreased acetylcholine-induced inward current in these neurons. NAN-190 and methiothepin, antagonists of 5-HT1 serotonin receptors, prevented this modulatory effect of 5-HT. By contrast, LY-53.857, ICS-205.930, and SDZ-205.557, antagonists of 5-HT2, 5-HT3, and 5-HT4 serotonin receptors, respectively, produced no effect on the modulatory effect of serotonin. The data confirm the presence of modulator 5-HT1 serotonin receptor on the soma of command neurons of Helix pomatia.

Acetylcholine↗
PubMed2000

Involvement of ryanodine receptors in EPYLRFamide-mediated reduction of acetylcholine-induced inward currents in helix lucorum identified neurones.

The effects of several modulators of ryanodine receptors (RYRs) on the reduction of acetylcholine induced inward current (ACh-current) evoked by EPYLRFamide (5 microM, bath application), the potent N-terminally modified analogue of the endogenous Helix heptapeptide SEPYLRFamide, were investigated. These modulators were applied intracellularly. Inward currents were recorded from identified Helix lucorum LPa2, LPa3, RPa3, RPa2 neurones in ganglia preparations using the two-electrode voltage clamp technique. ACh was applied ionophoretically. BAPTA (0.1 mM), chelator of intracellular Ca(2+), ryanodine (0.1 mM), agonist/antagonist of RYRs and dantrolene (0.1 mM), antagonist of RYRs decrease the effect of EPYLRFamide. Adenosine (1 mM), alpha,beta-methylene ATP (0.1 mM), the nonhydrolisable ATP analogue and cyclic adenosine diphosphate ribose (0.1 mM) (agonists of RYRs) potentiate the modulatory effect of EPYLRFamide. Ruthenium red (1 mM), antagonist of RYRs and caffeine (1 mM), agonist of RYRs do not change the modulatory effect of EPYLRFamide. These data suggest that intracellular Ca(2+) and RYRs are involved in the modulatory effect of EPYLRFamide on ACh-currents. It was concluded that EPYLRFamide decreases ACh-current through elevation of basal intracellular level of a putative endogenous agonist of RYRs which activates RYR-dependent mobilization of Ca(2+) by binding to the adenine nucleotide site of the ryanodine receptor-channel complex and does not bind the site activated by caffeine.

Acetylcholine↗
PubMed1999

Structure-activity relationships of the Helix neuropeptide, SEPYLRFamide, and its N-terminally modified analogues on identified Helix lucorum neurones.

Metabotropic and ionotropic effects evoked by the endogenous Helix heptapeptide, SEPYLRFamide, and four analogues, i.e., where the amino acid sequences at the N-terminal (EPYLRFamide, SEGYLRFamide, SRPYLRFamide and SKPYLRFamide) were modified, were compared on identified Helix lucorum LPa2, LPa3, RPa3, RPa2 neurones using two electrode voltage clamp and current clamp techniques. All peptides (bath application) reduce reversibly the inward current to local ionophoretic application of acetylcholine onto the neurone soma with an order of potency: EPYLRFamide=SEGYLRFamide=SRPYLRFamide>SEPYLRFamide+ ++>SKPYLRFamide. The reductions of the acetylcholine-induced inward current evoked by SEPYLRFamide and its analogues at concentrations of 0.01-10 microM are not accompanied by a change of amplitude of the leak inward current caused by constant negative shift of a holding potential. At concentration of 50 microM all peptides increase reversibly the resting membrane conductance to an equal degree. Local application under pressure of SEPYLRFamide and its analogues onto the soma of neurones evoke hyperpolarizations with similar values. These results indicate that the N-terminal three amino acids of the peptide molecule are not responsible for the degree of ionotropic effect on the neurones studied. In contrast the amino acid sequence at the N-terminal modifies the degree of the modulatory effects of the YLRFamide-related analogues. Changes at the SEPYLRFamide N-terminal (Ser1-Glu2-Pro3) intensify the inhibitory action of the analogues as compared with effect evoked by the endogenous peptide, that is, removal of Ser1 (Glu1-Pro2), replacement of Pro3 with Gly3 (Ser1-Glu2-Gly3), replacement of Glu2 with Arg2 (Ser1-Arg2-Pro3). Replacement of Glu2 with Lys2 (Ser1-Lys2-Pro3) reduces the modulatory potency. It is concluded that ionotropic and metabotropic effects of these YLRFamide-related peptides may occur at different membrane binding sites.

Acetylcholine↗
PubMed1996

Direct and modulatory effects of FMRFamide, SKPYMRFamide and acety1-SKPYMRFamide on LPa2, LPa3, and RPa3 identified neurons of Helix lucorum.

Three neuroactive peptides with an RFamide carboxyl terminal, one a tetrapeptide, FMRFamide, and two heptapeptides, SKPYMRFamide and acetyl-SKPYMRFamide, evoke direct and modulatory effects on identified neurons from left (LPa2, LPa3) and right (RPa3) parietal ganglia of the land snail. Helix lucorum. Local application of tetrapeptide and heptapeptides induce hyperpolarization or outward current when neurons are clamped at the resting potential. The reversal potential of these direct responses is near the potassium equilibrium potential. All investigated FMRFamide-related peptides reduce reversibly the inward current to local acetylcholine (ACh) application onto the neuron soma. Threshold concentrations of peptides for an inhibitory action on ACh-induced current are 0.5-1.0 microM, ID50 = 0.7-1.2 microM, SKPYMRFamide evokes parallel shift to right of ACh dose-response curves increasing the ED50 for ACh but without changing the Hill number. SKPYMRFamide does not change the reversal potential of the ACh-induced inward current. It was concluded that SKPYMRFamide reduces the affinity of ACh for ACh receptor without a change in the number of ligand-binding sites per ACh receptor molecule. FMRFamide-related peptides can reduce the affinity of ACh for cholinergic receptors through inhibition of the molecular mechanism connecting the ACh receptor with its ion channels.

Acetylcholine↗
PubMed1995

Inhibitory action of SKPYMRFamide on acetylcholine receptors of Helix aspersa neurons: role of second messengers.

1. SKPYMRFamide, a novel FMRFamide-like endogenous peptide reversibly decreases excitatory responses (depolarization and inward current) evoked by local ionophoretic application of acetylcholine (ACh) onto the soma of identified neurons F1, F2, F4 and F5/6 of the land snail, Helix aspersa. 2. Threshold concentrations of SKPYMRFamide for an inhibitory action on ACh-induced responses are 0.5-1 mumoll-1. This modulatory action of peptide is dose- and time-dependent. 3. It is concluded that SKPYMRFamide inhibits ACh receptors through activation of specific binding sites on the plasma membrane. 4. The possible role of different second messengers in the modulatory influence of SKPYMRFamide on ACh receptors was tested using 13 modulators of different second messenger systems. 5. The results indicate that SKPYMRFamide may inhibit ACh receptors through activation of one or more of the following systems: phospholipases C, A2, NO-synthase, soluble guanylate cyclase and lipoxygenases which elevate basal intracellulal levels of NO, cGMP, arachidonic acid, acyclic eicosanoids, inositol-1,4,5-trisphosphate (I(1,4,5)P3), I(1,4,5)P3-dependent Ca(2+)-mobilization followed by activation of calmodulin and Ca2+/calmodulin-dependent protein kinase II. Protein kinases A, C and cyclic eicosanoids do not appear to participate in modulatory action of SKPYMRFamide.

Acetylcholine↗
PubMed1995

Regulation of neuron cholinoreceptor plasticity of Helix lucorum by second messengers and opioids.

The rhythmical local ionophoretic applications of acetylcholine (ACh) to the somatic membrane of Helix lucorum identified neurons evokes the reversible depression of the ACh-induced response which shows cholinoreceptor (ChR) desensitization. ChR desensitization is regulated not by one but by several known second messengers and G-proteins. The endogenous opioids perform the excitation or inhibitory tonic control of the membrane potential in some neurons constantly activating the ionotropic opiate receptors. The direction of neuron ChR desensitization modulation by opioids depends on the type of the activated modulatory opiate receptors (mu or kappa) on the neuron membrane. Second messengers are involved in intracellular mechanism of modulation of the ChR desensitization by opiate kappa-agonist bremazocine.

Acetylcholine↗
PubMed1993

[A comparison of the effects of 5-hydroxyeicosatetraenoic acid and hepoxilin A3 on the plasticity of the snail neuronal cholinoreceptors].

The effects of two acyclic derivatives of arachidonic acid which are formed under the action of 5- and 12-lipoxygenases 5(S)-hydroxy-(6,8Z,11Z,14Z)-eicosatetraenoic acid (5-HETE) and (8R/S)-hydroxy-(11S,12S)-epoxy-5Z,9E,14Z-eicosatrienoi c acid (hepoxilin A3) on extinction of inward current evoked by local acetylcholine (ACh-current) application on soma of Helix lucorum RPa3 and LPa3 neurons were studied by the double-electrode voltage clamp technique. It was shown an increase in ACh-current extinction by 5-HETE. Hepoxilin A3 did not influence cholinoreceptor plasticity. The present results confirm earlier assumptions concerning the regulation of cholinoreceptor plasticity by acyclic eicosanoids which were formed from arachidonic acid under the influence of 5-lipoxygenase and the lack of 12-lipoxygenase metabolites in this regulation.

8,11,14-Eicosatrienoic Acid↗
PubMed1993

[The effect of a decrease in the mobilization of Ca+ and its chemo-controlled intake into the cytoplasm on the modulation of cholinoreceptor neuronal plasticity in Helix lucorum snails by 15-hydroxyeicosatetraenoic acid].

The effects of extracellular solution without Ca2+ and inhibitors of Ca2+ mobilization dependent of Ca2+ (tetracaine) and inositol-1,4,5-trisphosphate (TMB-8) on the modulation of cholinoreceptor (ChR) plasticity of identified Helix lucorum RPa3 and LPa3 neurons by 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE) were investigated. Using the double-electrode voltage-clamp technique, the inward current, induced by local ionophoretic acetylcholine application (ACh-current), was recorded. ChR plasticity was evaluated by extinction of ACh-current developed in a process of rhythmic ACh applications on the soma with an interval 60-240 s. Tetracaine and TMB-8 disturbed long-latent modulatory effect of 15-HETE and did not influence short-latent one. Extraction of Ca2+ from extracellular solution did not affect the modulatory effect of 15-HETE. It was concluded that one of the molecular mechanisms of ChR plasticity deepening due 15-HETE (in long-latent phase) induces potentiation of Ca(2+)- and inositol-1,4,5-trisphosphate-dependent Ca2+ mobilization evoked by 5-lipoxygenase eicosanoids.

Acetylcholine↗
PubMed1992

[Identification of cholinoreceptors on the soma of RPa3 and LPa3 neurons in Helix lucorum].

Selective cholinomimetics and cholinolytics were employed to identify cholinoreceptors on the somatic membrane in Helix lucorum RPa3 and LPa3 neurons using recording of transmembrane ionic currents. Agonists of nicotinic and muscarinic cholinoreceptors evoked reversible activation and following nonreversible inhibition of receptors (except carbamylcholine). Selective cholinomimetics were connected with the same membrane sites that were activated by acetylcholine. Nicotinic and muscarinic cholinolytics decreased the amplitude of inward current induced by acetylcholine (scopolamine and platyphylline had no effect). It is concluded that somatic membrane of RPa3 and LPa3 Helix neurons contains nicotinic and muscarinic cholinoreceptors. These receptors have several pharmacological peculiarities as compared with those of the vertebrates. Muscarinic cholinoreceptors of RPa3 and LPa3 neurons must be included into a special subtype that differs from well-known M1 and M2 subtypes.

Acetylcholine↗
PubMed1991

[Short and long latent effects of 15-hydroxyeicosatetraenoic acid on the extinction of the acetylcholine-induced inward current in neurons of the Helix lucorum].

The impact of a non-cyclized arachidonic acid derivative 15S-hydroxy-5Z, 8Z, 11Z, 13E-eicosatetraenoic acid (15-HETE) upon the dynamics of the inward current extinction, caused by repeated ion-tophoretic acetylcholine applications on the soma, was studied through a double electrode voltage clamp technique on the Helix lucorum identified neurons RPa3 and LPa3. The extracellular effect of 15-HETE (4-16 microM) was found to have a two phase influence on the inward current extinction, depending on the time of exposure to the compound. The short-latent effect (up to 60-80 min) displays itself as an extinction decrease, whereas the long-latent effect (after 60-80 min) - as an enhanced extinction. The effects caused by 15-HETE are irreversible. The short-latent one was probably due to the earlier described inhibition of 5- and 12-lipoxygenase enzymes by 15-HETE while the long-latent one - due to its intrinsic function.

Acetylcholine↗