Effect of nicotine on neuromuscular transmission in mouse motor synapses

Балезина, О. П.; Fedorin, V. V.; Gaidukov, A. E.

doi:10.1007/s10517-006-0280-3

Cited by 8 publications

(13 citation statements)

References 14 publications

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“…Thus, nicotine at a concentration of 10 μM exerts both postsynaptic and presynaptic inhibitory effects on the neuromuscular synapse, in particular, causing a decrease in the number of ACh quanta released in response to action potential. Similar decrease in the QC during activation of cholinergic receptors has been noted earlier (Tian et al, 1994;Prior & Singh, 2000;Balezina et al, 2006;Khaziev et al, 2016), however, these results were obtained on other preparations and in conditions of initially reduced QC, or in cut fiber preparations.…”

Section: Effects Of Nicotine On Ach Releasesupporting

confidence: 86%

“…Their activation is accompanied by depolarization of sarcolemma and subsequent generation of action potential, which ultimately leads to muscle contraction. The data collected by to date indicate that activation of presynaptic nicotinic cholinergic receptors leads to inhibition of the process of ACh release (Van der Kloot, 1993;Prior & Singh, 2000;Balezina et al, 2006). Also, experimental evidence was obtained indicating possible involvement of voltage-gated calcium channels (VGCCs) of L-type (Ca v 1) in modulation of neurotransmission (Prior & Singh, 2000).…”

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confidence: 99%

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Activation of neuronal nicotinic receptors inhibits acetylcholine release in the neuromuscular junction by increasing Ca2+ flux through Cav1 channels

Zhilyakov

Arkhipov

Malomouzh

et al. 2021

Preprint

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Background and Purpose: Cholinergic neurotransmission is a key signal pathway in the peripheral nervous system (PNS) and in several branches of the central nervous system (CNS). Despite the fact that it has been studied extensively for a long period of time, some aspects of its regulation still have not yet been established. One is relationship between nicotine-induced autoregulation of acetylcholine (ACh) release with changes in the concentration of presynaptic calcium levels. Experimental Approach: The mouse neuromuscular junction of m. Levator Auris Longus was chosen as the model of the cholinergic synapse. ACh release was assessed by electrophysiological methods. Changes in the calcium transients were recorded using a calcium-sensitive dye. Functional interaction between nicotinic ACh receptors and calcium channels was investigated pharmacologically using specific agonists and antagonists. Key Results: Nicotine hydrogen tartrate salt (considered as a stable form for potential therapeutic delivery of nicotine) effects on the parameters of ACh release from the nerve ending were analyzed. Nicotine application (10 μM) decrease the amount of evoked ACh release, while calcium transient increase in the motor nerve terminal. Both of these effects of nicotine were abolished by the neuronal ACh receptor antagonist dihydro-beta-erythroidine and Cav1 blockers, verapamil and nitrendipine. Conclusion and Implications: Neuronal nicotinic ACh receptors activation decreases the number of ACh quanta released by boosting calcium influx through Cav1 channels. Understanding of mechanisms of autoregulation of ACh release is important for the searching new approaches treat diseases associated with cholinergic dysfunction.

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Section: Effects Of Nicotine On Ach Releasesupporting

confidence: 86%

mentioning

confidence: 99%

Activation of neuronal nicotinic receptors inhibits acetylcholine release in the neuromuscular junction by increasing Ca2+ flux through Cav1 channels

Zhilyakov

Arkhipov

Malomouzh

et al. 2021

Preprint

View full text Add to dashboard Cite

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“…The dissection of muscle fiber allowing one to simultaneously record both a spontaneous and non-reduced evoked release of the neurotransmitter was performed according to the standard protocol [ 5 , 17 , 18 ]. The left half of the diaphragm with the phrenic nerve was put into a 3-mL camera and rinsed with an oxygenated (95% O2, 5% CO 2 ) Liley buffer (pH 7.2–7.4, 135 mM NaCl, 4 mM KCl, 0.9 mM NaH 2 PO 4 , 2 mM CaCl 2 , 1 mM MgCl2, 16.3 mM NaHCO 3 , 11 mM glucose) at room temperature.…”

Section: Methodsmentioning

confidence: 99%

“…In contrast to the central nervous system where activation of presynaptic α7-nAChRs with ACh or selective agonists (choline, nicotine) typically facilitates neurotransmitter release [ 13 - 16 ], inhibition of the release in peripheral motor synapses has been reported [ 5 , 17 ]. In our previous research, activation of α7-nAChRs with small doses of nicotine triggered calcium-dependent inhibition of the evoked release of acetylcholine in rhythmically stimulated neuromuscular junctions of mouse, which could be prevented by using methyllycaconitine, a selective antagonist of α7-nAChRs [ 18 ]. The mechanisms of this inhibition remain unclear.…”

Section: Introductionmentioning

confidence: 99%

The Mechanism of Choline-Mediated Inhibition of Acetylcholine Release in Mouse Motor Synapses

et al. 2014

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The mechanism of action of tonically applied choline, the agonist of α7 nicotinic acetylcholine receptors (nAChRs), to the spontaneous and evoked release of a neurotransmitter in mouse motor synapses in diaphragm neuromuscular preparations using intracellular microelectrode recordings of miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) was studied. Exogenous choline was shown to exhibit a presynaptic inhibitory effect on the amplitude and quantal content of EPPs for the activity of neuromuscular junction evoked by single and rhythmic stimuli. This effect was inhibited either by antagonists of α7-nAChRs, such as methyllycaconitine and α-cobratoxin, or by blocking SK-type calcium-activated potassium (KCa) channels with apamin or blocking intraterminal ryanodine receptors with ryanodine. A hypothesis was put forward that choline in mouse motoneuron nerve terminals can activate presynaptic α7-nAChRs, followed by the release of the stored calcium through ryanodine receptors and activation of SK-type KCa channels, resulting in sustained decay of the quantal content of the evoked neurotransmitter release.

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“…Their activation is accompanied by the depolarization of sarcolemma and the subsequent generation of action potential, which ultimately leads to muscle contraction. The data indicate that the activation of presynaptic nicotinic cholinergic receptors leads to inhibition of the process of ACh release [19][20][21].…”

Section: Introductionmentioning

confidence: 88%

Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca2+ Flux through Cav1 Channels

Zhilyakov

Arkhipov

Malomouzh

et al. 2021

IJMS

View full text Add to dashboard Cite

Cholinergic neurotransmission is a key signal pathway in the peripheral nervous system and in several branches of the central nervous system. Despite the fact that it has been studied extensively for a long period of time, some aspects of its regulation still have not yet been established. One is the relationship between the nicotine-induced autoregulation of acetylcholine (ACh) release with changes in the concentration of presynaptic calcium levels. The mouse neuromuscular junction of m. Levator Auris Longus was chosen as the model of the cholinergic synapse. ACh release was assessed by electrophysiological methods. Changes in calcium transients were recorded using a calcium-sensitive dye. Nicotine hydrogen tartrate salt application (10 μM) decreased the amount of evoked ACh release, while the calcium transient increased in the motor nerve terminal. Both of these effects of nicotine were abolished by the neuronal ACh receptor antagonist dihydro-beta-erythroidine and Cav1 blockers, verapamil, and nitrendipine. These data allow us to suggest that neuronal nicotinic ACh receptor activation decreases the number of ACh quanta released by boosting calcium influx through Cav1 channels.

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Effect of nicotine on neuromuscular transmission in mouse motor synapses

Abstract: Nicotine (10 nM) inhibits rhythmic activity of the neuromuscular synapse in mice. This effect was prevented by alpha-cobratoxin and apamin. Hence, the effects of nicotine are realized via presynaptic neuronal nicotinic cholinoceptors and Ca(2+)-activated potassium channels.

Cited by 8 publications

References 14 publications

Activation of neuronal nicotinic receptors inhibits acetylcholine release in the neuromuscular junction by increasing Ca2+ flux through Cav1 channels

Activation of neuronal nicotinic receptors inhibits acetylcholine release in the neuromuscular junction by increasing Ca2+ flux through Cav1 channels

The Mechanism of Choline-Mediated Inhibition of Acetylcholine Release in Mouse Motor Synapses

Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca2+ Flux through Cav1 Channels

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