Metabotropic and ionotropic glutamate receptors mediate the modulation of acetylcholine release at the frog neuromuscular junction

© 2016 Wiley Periodicals, Inc.There is some evidence that glutamate (Glu) acts as a signaling molecule at vertebrate neuromuscular junctions where acetylcholine (ACh) serves as a neurotransmitter. In this study, performed on the cutaneous pectoris muscle of the frog Rana ridibunda, Glu receptor mechanisms that modulate ACh release processes were analyzed. Electrophysiological experiments showed that Glu reduces both spontaneous and evoked quantal secretion of ACh and synchronizes its release in response to electrical stimulation. Quisqualate, an agonist of ionotropic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptors and metabotropic Group I mGlu receptors, also exerted Glu-like inhibitory effects on the secretion of ACh but had no effect on the kinetics of quantal release. Quisqualate's inhibitory effect did not occur when a blocker of Group I mGlu receptors (LY 367385) or an inhibitor of phospholipase C (U73122) was present. An increase in the degree of synchrony of ACh quantal release, such as that produced by Glu, was obtained after application of N-methyl-D-aspartic acid (NMDA). The presence of Group I mGlu and NMDA receptors in the neuromuscular synapse was confirmed by immunocytochemistry. Thus, the data suggest that both metabotropic Group I mGlu receptors and ionotropic NMDA receptors are present at the neuromuscular synapse of amphibians, and that the activation of these receptors initiates different mechanisms for the regulation of ACh release from motor nerve terminals. © 2016 Wiley Periodicals, Inc

Presynaptic nicotinic cholinoreceptors modulate velocity of the action potential propagation along the motor nerve endings at a high-frequency synaptic activity

© 2016, Pleiades Publishing, Ltd.Experiments on frog neuromuscular junctions have demonstrated that asynchrony of the acetylcholine quantal release forming the multi-quantal evoked response at high-frequency synaptic activity is caused, in particular, by a decrease in velocity of the action potential propagation along the non-myelinated nerve endings, which is mediated by activation of the α7 and α4β4 nicotinic cholinoreceptors

Effect of Noradrenaline on the Kinetics of Evoked Acetylcholine Secretion in Mouse Neuromuscular Junction

© 2018, Pleiades Publishing, Ltd. Abstract: In contrast to frog neuromuscular synapses, where noradrenaline (norepinephrine) and its analogues caused synchronization of the acetylcholine release process, in mouse diaphragm endplates noradrenaline increased the degree of asynchrony of neurosecretion. The effect of noradrenaline on release timing persisted at different levels of external calcium ions (0.25–2.0 mM) and was abolished in presence of both α- and β‑adrenoblockers phentolamine and propranolol. The computer reconstruction of multiquantal endplate currents accounting for experimentally observed modification of release kinetics under noradrenaline showed that the rise time of postsynaptic response changes to a greater extent than the amplitude and falling phase of the multiquantal responses. We conclude that there exists a principal difference in the action of noradrenaline in the cholinergic neuromuscular synapses of warm-blooded and cold-blooded animals that can be accounted for by the differences in the type of adrenoreceptors involved in the modulation of synaptic transmission and/or in the involvement of distinct intracellular pathways triggered by receptor activation

Muscarinic cholinoreceptors (M1-, M2-, M3- and M4-type) modulate the acetylcholine secretion in the frog neuromuscular junction

© 2017 Elsevier B.V.Muscarinic cholinoreceptors regulate the neurosecretion process in vertebrate neuromuscular junctions. The diversity of muscarinic effects on acetylcholine (ACh) secretion may be attributed to the different muscarinic subtypes involved in this process. In the present study, the location of five muscarinic receptor subtypes (M1, M2, M3, M4 and M5) on the motor nerve terminals of frog cutaneous pectoris muscle was shown using specific polyclonal antibodies. The modulatory roles of these receptors were investigated via assessment of the effects of muscarine and specific muscarinic antagonists on the quantal content of endplate currents (EPCs) and the time course of secretion, which was estimated from the distribution of “real” synaptic delays of EPCs recorded in a low Ca2+/high Mg2+ solution. The agonist muscarine decreased the EPC quantal content and synchronized the release process. The depressing action of muscarine on the EPC quantal content was abolished only by pretreatment of the preparation with the M3 blockers 4-DAMP (1,1-Dimethyl-4-diphenylacetoxypiperidinium iodide) and J 104129 fumarate ((αR)-α-Cyclopentyl-α-hydroxy-N-[1-(4-methyl-3-pentenyl)-4-piperidinyl]benzeneacetamide fumarate). Moreover, antagonists of the M1, M2, M3 and M4 receptors per se diminished the intensity of secretion, which suggests a putative up-regulation of the release by endogenous ACh

Calcium modulation of the kinetics of evoked quantum secretion in neuromuscular synapses of cold- and warm-blooded animals

© 2015, Pleiades Publishing, Ltd. Calcium entry into the nerve endings through voltage-dependent calcium channels triggers a chain of events leading to exocytosis of neurotransmitter, providing the transmission of excitation through the synapse. In this regard, a significant role of calcium ions and presynaptic calcium channels in the modulation of secretion is evident. However, the question of the contribution of different types of voltage-dependent calcium channels in the calcium regulation parameters of the quantal secretion still remains unclear. The secretion kinetics characterizes a degree of synchrony of the neurotransmitter release. In recent decades it is regarded as one of the important factors maintaining the effectiveness of the synaptic transmission. Since neuromuscular synapses of frogs and mice are classical objects of physiological and pharmacological studies, the results of which are summarized and extrapolated to other synapses, it is interesting to compare changes of the acetylcholine secretion in these synapses under different conditions of calcium entry into the nerve endings. In this review we discuss the data on the neuromuscular synapses of frogs and mice and analyze some aspects of calcium regulation and involvement of different types of voltage-dependent calcium channels in the modulation of the acetylcholine secretion kinetics

Polysaccharides of cell wall of wheat roots under extreme growth conditions

Incorporation of radioactivity from 14CO 2 into various fractions and polysaccharides of the cell wall of wheat germ roots was analyzed after 40-min photosynthesis and subsequent 24-h growth. Radioactivity of cell wall polysaccharides was decreased by 50-70% during 10-day adaptation of isolated roots under extreme growth conditions. Pectines and alkali-soluble hemicelluloses of the cell wall can be used as reserved sources of endogenous nutrition of root cells during chronic starvation. Insignificant decrease in radioactivity of structural polysaccharides after 14-day incubation of isolated roots can be an indicator of cellular degradation (according to membrane potential)

Presynaptic nicotinic cholinoreceptors modulate velocity of the action potential propagation along the motor nerve endings at a high-frequency synaptic activity

© 2016, Pleiades Publishing, Ltd.Experiments on frog neuromuscular junctions have demonstrated that asynchrony of the acetylcholine quantal release forming the multi-quantal evoked response at high-frequency synaptic activity is caused, in particular, by a decrease in velocity of the action potential propagation along the non-myelinated nerve endings, which is mediated by activation of the α7 and α4β4 nicotinic cholinoreceptors

Presynaptic nicotinic cholinoreceptors modulate velocity of the action potential propagation along the motor nerve endings at a high-frequency synaptic activity

© 2016, Pleiades Publishing, Ltd.Experiments on frog neuromuscular junctions have demonstrated that asynchrony of the acetylcholine quantal release forming the multi-quantal evoked response at high-frequency synaptic activity is caused, in particular, by a decrease in velocity of the action potential propagation along the non-myelinated nerve endings, which is mediated by activation of the α7 and α4β4 nicotinic cholinoreceptors

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Effect of Noradrenaline on the Kinetics of Evoked Acetylcholine Secretion in Mouse Neuromuscular Junction

© 2018, Pleiades Publishing, Ltd. Abstract: In contrast to frog neuromuscular synapses, where noradrenaline (norepinephrine) and its analogues caused synchronization of the acetylcholine release process, in mouse diaphragm endplates noradrenaline increased the degree of asynchrony of neurosecretion. The effect of noradrenaline on release timing persisted at different levels of external calcium ions (0.25–2.0 mM) and was abolished in presence of both α- and β‑adrenoblockers phentolamine and propranolol. The computer reconstruction of multiquantal endplate currents accounting for experimentally observed modification of release kinetics under noradrenaline showed that the rise time of postsynaptic response changes to a greater extent than the amplitude and falling phase of the multiquantal responses. We conclude that there exists a principal difference in the action of noradrenaline in the cholinergic neuromuscular synapses of warm-blooded and cold-blooded animals that can be accounted for by the differences in the type of adrenoreceptors involved in the modulation of synaptic transmission and/or in the involvement of distinct intracellular pathways triggered by receptor activation