PubMed Health⌕ Search

Biomedical subjects

E I Drozdova

Publications and source records attributed to E I Drozdova.

At least 19 recordsLinked to original sources
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↗
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↗
PubMed1989

[Second messengers in the regulation of nerve cell plasticity during learning].

A review of 1972 to 1988 publications is presented, as well the data obtained by the authors on the influence of second messengers and their intracellular receptors on neuron plasticity in the learning experimental models. The emphasis is laid on cyclic 3',5'-adenosine monophosphate; cyclic 3',5'-guanosine monophosphate, calcium ions and their intracellular receptor calmodulin, as well as on the metabolites of phosphoinositide exchange: inositol-1, 4, 5-trisphosphate, 1,2-diacylglycerol and protein kinase C activated by the latter and arachidonic acid.

Animals↗
PubMed1989

[Protein kinase C is not involved in regulating the short-term cholinoreceptor plasticity of the PPa3 and LPa3 neurons of the edible snail].

A voltage clamp technique on identified Helix lucorum's RPa3 and LPa3 neurons has been used to negate the effect of protein kinase C on extinction of response to repeated iontophoretic applications of acetylcholine to soma. Extracellular influence of phorbol ether, protein kinase C activator (12-O-tetradecanoylphorbol-13-acetate, 0.1-10 mumol/l), or polymyxin B, its blocker (100-500 mumol/l), do not affect the extinction of acetylcholine-induced neuronal response. The data show that protein kinase C is not involved into molecular mechanisms responsible for the regulation of short-term plasticity of RPa3 and LPa3 neuronal cholinoreceptors in Helix lucorum.

Acetylcholine↗
PubMed1988

[The role of cyclic 3',5'-adenosine monophosphate in the extinction of the reaction of identified neurons in the edible snail to acetylcholine].

The recording of transmembrane currents and intracellular potentials has been used to show on Helix lucorum identified neurons RPa4, RPa3 and LPa3, that pharmacologic effects on adenylate cyclase system do not influence the extinction of neuronal response to repeated local iontophoretic applications of acetylcholine to the soma. Neither cAMP-raising adenylate cyclase activator forskolin (2-6 x 10(-5) mol/l), nor cAMP-lowering phosphodiesterase activator imidazole (5 x 10(-3) mol/l) alter the dynamics of extinction of response to acetylcholine. A conclusion has been made that shortterm plasticity of cholinoreceptors in the investigated neurons is independent of intracellular cAMP level.

Acetylcholine↗
PubMed1987

[Effect of piracetam on the habituation of the neuronal cholinoreceptor membrane of the edible snail].

Piracetam is shown to modulate the habituation pattern of cholinoreceptor neuronal membrane in Helix lucorum. Piracetam (10(-2) M) intensified the reversible decrease of depolarization and spike discharge induced by the local microionophoretic rhythmical application of acetylcholine to the neuron soma. The ability of piracetam to intensify the habituation of neuronal cholinoreceptor membrane may serve as a model of its facilitating effect on the development of habituation of behavioural reactions. Piracetam (5.10(-2) M) was shown to induce a shift in the membrane potential towards depolarization in the majority of identified neurons studied.

Acetylcholine↗
PubMedDate not supplied

Arachidonic acid and its acyclic derivatives regulate short-term plasticity of the cholinoreceptors of neurons of the edible snail.

The influence of eicosanoids on the dynamics of the extinction of the inward current, induced by repeated iontophoretic applications of acetylcholine to the soma has been demonstrated in identified RPa3 and LPa3 neurons of the edible snail by means of bielectrode recording of the membrane potential. The extracellular action of arachidonic acid (50-100 mumole/l) intensifies the extinction. Quinacrine (100-600 mumole/l), an inhibitor of phospholipase A2, which decreases the content of arachidonic acid in the cells, acts ambiguously. Nordihydroguaiaretic acid (3-10 mumole/l), which is an inhibitor of the lipoxygenase oxidation of arachidonic acid, attenuates the extinction. Indomethacin (10-50 mumole/l), a blocker of cyclooxygenase oxidation of arachidonic acid, does not influence extinction. All of the compounds investigated decrease the amplitude of the inward current induced by acetylcholine. The results obtained make it possible to hypothesize that arachidonic acid and its acyclic metabolites, which are formed as a result of lipoxygenase oxidation, regulate short-term plasticity of the cholinoreceptors of neurons of the edible snail. The cyclic eicosanoids which are formed during the cyclooxygenase oxidation of arachidonic acid do not exert a regulatory effect on the plasticity of the cholinoreceptors.

Animals↗
PubMedDate not supplied

Eicosapolyynoic acids, inhibitors of lipoxygenases, weaken the short-term plasticity of cholinoreceptors of neurons of the edible snail.

The influence of three polyacetylenic analogs of natural polyenoic acids which are inhibitors of their lipoxygenase oxidation on the dynamics of the extinction of the inward current induced by repeated iontophoretic applications of acetylcholine to the soma was investigated in identified RPa3 and LPa3 of the edible snail using the method of bielectrode recording of the potential on the membrane. It was found that eicosa-5,8,11,14-tetraynoic acid (30-60 mumole/liter) and eicosa-5,8,11,14,17-pentaynoic acid (4-50 mumole/liter) decrease the amplitude of the inward current induced by application of acetylcholine, and attenuate its extinction during repeated applications. The third analog, eicosa-8,11,14-triaynoic acid, does not exert a modulating influence on the magnitude of the current and its extinction. It was hypothesized that the lipoxygenase metabolites of the polyenoic acids regulate the plasticity of the cholinoreceptors of the neurons of the edible snail. Taking the nonidentical inhibition by the compounds used of the various lipoxygenases into account, the participation in the plasticity of the cholinoreceptors of those eicosanoids which are formed from arachidonic acid under the influence of 5-lipoxygenases is most probable. At the same time, a regulatory role of the eicosanoids formed under the influence of other lipoxygenases is not excluded.

5,8,11,14-Eicosatetraynoic Acid↗
PubMedDate not supplied

Calmodulin blockers decrease short-term plasticity of the cholinoreceptors of neurons of the edible snail.

A reversible decrease in the rate and depth of the extinction of the reactions of the cholinoreceptive membrane to repeated iontophoretic applications of acetylcholine to the soma by a number of calmodulin blockers was demonstrated in identified RPa3 and LPa3 neurons in the edible snail using the method of recording transmembrane ionic currents: R 24571 (20-50 mumols/liter), trifluoperazine (50-200 mumols/liter), chlorpromazine (20-60 mumols/liter), and prenylamine lactate (30-400 mumols/liter). The results obtained attest to the positive regulation of short-term plasticity of the cholinoreceptors of the neurons in question by calmodulin.

Acetylcholine↗
PubMedDate not supplied

The role of cGMP in the extinction of the reactions of identified neurons of the edible snail in response to acetylcholine.

The possible role of cGMP in the regulation of the extinction of the reactions of the RPa4, RPa3, and LPa3 neurons of the edible snail in response to acetylcholine (ACh), applied rhythmically to the soma of the neuron by means of microiontophoresis, has been investigated. It was demonstrated that activators of guanylate cyclase which increased the level of cGMP in the cell, namely, sodium nitroprusside and sodium azide (5.10(-4)-10(-3) mole/liter), when applied intracellularly, intensify the extinction of inward transmembrane current and of depolarization of the membrane in response to ACh. The hypothesis of the participation of cGMP-dependent phosphorylation of membrane proteins in the regulation of the rate of development, depth, and duration of short-lived plasticity of the cholinoreceptors of the neuron is proposed.

Acetylcholine↗
PubMedDate not supplied

Amiridin and tacrine modulation of the activity and plasticity of the cholinoreceptors of neurons of the common snail: phenomenology and mechanisms.

The influence of amiridin and tacrine on the membrane potential, activity, and plasticity of cholinoreceptors was investigated using the methods of recording of intracellular potentials and transmembrane currents in identified RPa3 and LPa3 neurons of the common snail. Amiridin and tacrine (1-100 mumole/liter) do not exert appreciable influences on the membrane potential of the cells. Both compounds modulate the activity of cholinoreceptors, judging from their influence on the inward current induced by local application of the acetylcholine: the duration of the ACh current increases and its amplitude varies biphasically (a short-latency increase is succeeded by a decrease). Amiridin and tacrine intensify the extinction of the ACh current induced by repeated applications of ACh to the soma. The acetylcholinesterase inhibitor, physostigmine, exerts a similar modulatory influence on the ACh current and on its extinction, and also prevents the manifestation of the effects of amiridin and tacrine. Amiridin and physostigmine directly influence the cholinoreceptors and the ionic membrane channels controlled by them by similarly altering the voltage-current characteristics (VAC) of the ACh current, and by shifting the reversal potential of the ACh current in the negative direction, bringing it closer to the equilibrium potential for chloride ions; this may be interpreted as a result of the nonidentical action of these compounds on the various ionic currents controlled by cholinoreceptors. The hypothesis is advanced that the modulatory influence of amiridin, tacrine, and physostigmine on the activity and plasticity of the cholinoreceptors is governed by their direct membrane-cytoplasmic action.

Acetylcholine↗
PubMedDate not supplied

Ca-dependent regulation of the Na-K-pump by post-tetanic sensitization of extrasynaptic cholinoreceptors in common snail neurons.

Studies were conducted on the role of the Na,K pump and intracellular calcium in the previously observed phenomenon of increased cholinosensitivity of the somatic membranes of neurons LPa3 and RPa3 in the common snail, induced by electrical tetanic stimulation (10.5 mA. 0.1 sec, 2 impulses/sec; 2 min) of the afferent input (the intestinal nerve). Recordings were made of integral transmembrane acetylcholine-evoked currents by two-electrode membrane voltage clamping. After intracellular administration of the Na,K pump inhibitor ouabain (70 microM), there was no post-tetanic increase in neuron cholinosensitivity. Intracellular injection of the calcium ion chelator BAPTA suppressed the sensitization of somatic cholinoreceptors after orthodromal tetanization. It was concluded that the Na,K pump is involved in the mechanism of post-tetanic potentiation of cholinosensitivity in the bodies of defensive behavior command neurons in the common snail, this involvement being Ca-dependent.

Acetylcholine↗
PubMedDate not supplied

Generalized post-tetanic changes in excitatory postsynaptic and acetylcholine-evoked currents in neurons in the common snail.

Changes in excitatory postsynaptic currents (EPSC) and influx currents induced by local iontophoretic application of acetylcholine (ACh currents) to the surfaces of the bodies of identified neurons LPa3 and RPa3 in the common snail after heteroreceptor tetanic stimulation were studied. The effects of rhythmic application of acetylcholine (0.5-1.0 times per sec for 10-40 sec) on the magnitude of EPSC were analyzed, along with the effects of tetanic stimulation of the nerves (n. intestinalis, n. pallialis dexter, n. pallialis sinister; 1-5 Hz for 1-2 min) on the amplitudes of the ACh current and the magnitudes of EPSC evoked by stimulation of another nerve. The following changes in conditioning responses were found over 1-1.5 h after tetanization: rhythmic application of ACh to the dorsal surface of the cell body resulted in potentiation of EPSC, and tetanic orthodromic stimulation potentiated the ACh current and induced heterosynaptic depression of EPSC. These post-tetanic changes were not local--they developed in those chemoreceptor zones of the membrane which were not activated by the preceding conditioning rhythmic stimulation. It is concluded that generalized post-tetanic changes in neuron responses are induced by activation of its subsynaptic and extrasynaptic mediator chemoreceptors.

Acetylcholine↗
PubMedDate not supplied

[Generalized posttetanic changes in the excitatory postsynaptic and acetylcholine-evoked currents in snail neurons].

Heteroreceptor posttetanic changes in excitatory postsynaptic currents (EPSC) and inward currents evoked by the local iontophoretic application of acetylcholine (ACh) on the dorsal surface of PLa3 and PRa3 Helix lucorum neurons were studied. The following changes in the currents were revealed over the course of 1-1.5 h after tetanization. The rhythmical ACh application (0.5-1.0 cps, 10-40 s) evokes potentiation of the orthodromic EPSC. The tetanic orthodromic stimulation of one of the nerves (n. intestinalis, n. pallialis dexter, or n. pallialis sinister; 1-5 cps, 1-2 min) causes the potentiation of the ACh current and also heterosynaptic depression of the EPSC. It is concluded that activation of subsynaptic and nonsynaptic neurotransmitter chemoreceptors evokes the development of generalized posttetanic changes in neuronal responses.

Acetylcholine↗