Postsynaptic potentiation and desensitization at the frog neuromuscular junction produced by repeated stimulation of the motor nerve

Giniatullin, Rashid; Bal'tser, S. K.; Никольский, Е. Е.; Lg, Magazanik

doi:10.1007/bf01057817

Cited by 4 publications

(7 citation statements)

References 12 publications

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“…This, however, does not exclude the possibility that postsynaptic forms of plasticity such as postsynaptic potentiation and desensitization could be affected. Thus, further studies addressed the effects of sodium nitroprusside on conduction of rhythmic series of multiquantum endplate currents in conditions of acetylcholinesterase inhibition, when the postsynaptic phenomena of potentiation and desensitization are most marked [2].…”

Section: Resultsmentioning

confidence: 99%

“…In the presence of sodium nitroprusside at concentrations producing strong inhibitory effects on the amplitude of multiquantum endplate currents, this compound had no effect on either the amplitude or the decay time constant of the miniature current. The actions of many modifiers of postsynaptic electrogenesis are seen only in conditions of hyperpolarization of the postsynaptic membrane [2]. Therefore, the effects of sodium nitroprusside on voltage-dependent miniature endplate currents were studied in the next series of experiments.…”

Section: Resultsmentioning

confidence: 99%

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The effects of sodium nitroprusside on mediator release and the functional properties of postsynaptic membranes in the neuromuscular synapse

Зефиров

Khaliullina

Sokolova

et al. 2000

Neurosci Behav Physiol

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Experiments on neuromuscular preparations of frog skin- thoracic muscle and sartorius muscle, using extracellular recording and two-electrode clamping of the muscle fiber membrane potential, were used to study the effects of the nitric oxide donor sodium nitroprusside on endplate currents. At a concentration of 100 microM, sodium nitroprusside sharply decreased the amplitude and quantum composition of the endplate currents, and also decreased the miniature endplate current frequency. The amplitude-time characteristics of miniature endplate currents, the voltage-dependent amplitude, and the decay time constant of miniature endplate currents did not change as compared with controls. However, unlike the situation with other secretion inhibitors, the decrease in endplate current amplitude was not accompanied by increased facilitation in response to rhythmic stimulation or changes in postsynaptic potentiation in conditions of application of pairs of stimuli to muscles. The suppression of acetylcholine secretion was not seen with inactivated sodium nitroprusside solution. These results provide evidence that nitric oxide can be a powerful inhibitor of both spontaneous and evoked transmitter secretion in the neuromuscular synapse, and that this is accompanied by decreases in the efficiency of presynaptic forms of short-term plasticity, while the functional characteristics of the postsynaptic membrane remain unchanged.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

The effects of sodium nitroprusside on mediator release and the functional properties of postsynaptic membranes in the neuromuscular synapse

Зефиров

Khaliullina

Sokolova

et al. 2000

Neurosci Behav Physiol

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“…A desensitization-like phenomenon was observed during a sufficiently long period of nerve stimulation, namely 30-60 s (Magleby & Pallotta, 1981;Giniatullin et al 1986) with a high frequency, in particular after AChE inhibition. Desensitization onset is potentiated by muscle fibre hyperpolarization (Magazanik & Vyskocil, 1970), by increasing the temperature (Magazanik & Vyskocil, 1975) and by raising the concentration of divalent cations in the extracellular solution (Manthey, 1966;Magazanik & Vyskocil, 1970).…”

Section: R a Giniatullin And Othersmentioning

confidence: 99%

“…Nikolsky & Magazanik, 1986). A desensitization-like phenomenon was observed during a sufficiently long period of nerve stimulation, namely 30-60 s (Magleby & Pallotta, 1981;Giniatullin et al 1986) with a high frequency, in particular after AChE inhibition.…”

Section: R a Giniatullin And Othersmentioning

confidence: 99%

Development of desensitization during repetitive end‐plate activity and single end‐plate currents in frog muscle.

Giniatullin

Khamitov

Khazipov

et al. 1989

The Journal of Physiology

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SUMMARY1. The amplitudes of end-plate currents (EPCs) in short trains of fifteen to seventeen EPCs at 10 Hz were depressed in the presence of 10 ,uM-proadifen when acetylcholinesterase (AChE) was inhibited.2. The proadifen-induced EPC depression was voltage-dependent and the effect was more pronounced at negative membrane potentials.3. In the presence of proadifen, the mean amplitude of miniature end-plate currents (MEPCs) was reduced by 36% 5 s after the EPC train as compared with MEPCs before the train.4. Without proadifen, but with inhibited AChE, an increase of temperature from 20 to 26°C and elevation of external Ca2+ from 1-8 to 2-5 mm led to EPC amplitude depression in the train, which was also potential-dependent.5. After AChE inhibition, proadifen (10,uM) progressively shortened MEPC decay without significant reduction of amplitude up to 40 min of exposition. MEPCs were not affected by proadifen when AChE was active.6. It is concluded that these postsynaptic effects of proadifen can be explained neither by its action on the resting acetylcholine receptors (AChR) nor on open ion channels but are due to its desensitization-promoting action.

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“…A functional consequence of the high affinity shown by desensitized receptors is prevented reactivation of free receptors by the transmitter. Desensitized receptors may appear on the postsynaptic membrane in the course of rhythmic activity [2,5,12] and in the presence of ACh released in the nonquantum form [6]. This suggests that the effects of desensitized receptors that we have described may develop during functioning of the neuromuscular apparatus in vivo.…”

Section: Resultsmentioning

confidence: 94%

Physiological role of desensitized cholinoceptors in skeletal muscle

Giniatullin

Talantova

1995

Bull Exp Biol Med

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The effect of desensitized cholinoceptors on the time course of end-plate currents was evaluated in frog skeletal muscle at a high (physiological) level of acetylcholine secretion in the presence of active acetylcholinesterase, with two-electrode recording of the membrane potential. When the number of cholinoceptors was small so that they did not appreciably affect the amplitude of end-plate currents or the parameters of onequantum responses (miniature currents), the decay of multiquantum currents was significantly accelerated. Moreover, the presence of cholinoceptors drastically reduced the ability of acetylcholinesterase inhibitors to prolong the decay of end-plate currents. It is suggested that desensitized cholinoceptors in a synapse with a physiological level of acetylcholine secretion and active acetylcholinesterase may bind free acetylcholine with high affinity and thus supplement the well-known physiological role of acetylcholinesterase in limiting the reactivation of postsynaptic membrane cholinoceptors. Key Words: synapse; acetylcholine; desensitizationDesensitization of a muscle cell membrane, i.e., its reduced sensitivity to the neurotransmitter acetylcholine (ACh), may be induced by exogenous cholinomimetics, including depolarizing myorelaxants [10], and by the endogenous ACh released from nerve endings [5,6,12]. How desensitization affects the parameters of synaptic signals and what the functional role of this phenomenon is in skeletal muscle have not been ascertained. Desensitization, if strong, appears to be manifested in lowered amplitudes of synaptie signals as a result of a decrease in the number of receptors capable of opening ion channels when ACh is active. It has also been suggested that desensitized receptors may play a functional role in the redistribution of free ACh in the synaptic cleft through high-affinity binding of the transmitter [13]. Evidence in support of this hypothesis has so far been obtained only for muscles with inhibited acetylcholinesterase and low levels of ACh secretion. In view of this, we tried in this study to elucidate the functional role of desensitized receptors in the presence of active acetylcholinesterase and a high (physiological) level of ACh secretion, i.e., under conditions that, like acetylcholinestemse inhibition, increase the local concentration of this transmitter in the synaptic cleft as compared to its level in the case of one-quantum responses. MATERIALS AND METHODSThe experiment was conducted on neuromuscular preparations of the sciatic nerve-sartorius muscle from Rana ridibunda frogs, with two-electrode recording of the membrane potential. The muscle was continuously peffused with physiological solution of the following composition (mmol/liter): NaC1 113, KC1 2.5, CaC12 1.8, NaHCO 3 2.4; pH 7.2-7.4. To maintain the induced ACh secretion at a high level close to the physiological one, muscle contractions were prevented by transecting the muscle [1]. The nerve was stimulated at a fre-

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Postsynaptic potentiation and desensitization at the frog neuromuscular junction produced by repeated stimulation of the motor nerve

Cited by 4 publications

References 12 publications

The effects of sodium nitroprusside on mediator release and the functional properties of postsynaptic membranes in the neuromuscular synapse

The effects of sodium nitroprusside on mediator release and the functional properties of postsynaptic membranes in the neuromuscular synapse

Development of desensitization during repetitive end‐plate activity and single end‐plate currents in frog muscle.

Physiological role of desensitized cholinoceptors in skeletal muscle

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