Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels
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 th...
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doaj-aaab994dba58430c845c9ee6733c428c2021-08-26T13:53:42ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-08-01229031903110.3390/ijms22169031Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 ChannelsNikita Zhilyakov0Arsenii Arkhipov1Artem Malomouzh2Dmitry Samigullin3Kazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center, Russian Academy of Sciences, P.O. Box 261, 420111 Kazan, RussiaKazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center, Russian Academy of Sciences, P.O. Box 261, 420111 Kazan, RussiaKazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center, Russian Academy of Sciences, P.O. Box 261, 420111 Kazan, RussiaKazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center, Russian Academy of Sciences, P.O. Box 261, 420111 Kazan, RussiaCholinergic 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 Ca<sub>v</sub>1 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 Ca<sub>v</sub>1 channels.https://www.mdpi.com/1422-0067/22/16/9031neuromuscular junctionneurotransmitter releaseacetylcholinenicotinic receptorcalcium channelcalcium transient |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Nikita Zhilyakov Arsenii Arkhipov Artem Malomouzh Dmitry Samigullin |
spellingShingle |
Nikita Zhilyakov Arsenii Arkhipov Artem Malomouzh Dmitry Samigullin Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels International Journal of Molecular Sciences neuromuscular junction neurotransmitter release acetylcholine nicotinic receptor calcium channel calcium transient |
author_facet |
Nikita Zhilyakov Arsenii Arkhipov Artem Malomouzh Dmitry Samigullin |
author_sort |
Nikita Zhilyakov |
title |
Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels |
title_short |
Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels |
title_full |
Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels |
title_fullStr |
Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels |
title_full_unstemmed |
Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca<sup>2+</sup> Flux through Ca<sub>v</sub>1 Channels |
title_sort |
activation of neuronal nicotinic receptors inhibits acetylcholine release in the neuromuscular junction by increasing ca<sup>2+</sup> flux through ca<sub>v</sub>1 channels |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1661-6596 1422-0067 |
publishDate |
2021-08-01 |
description |
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 Ca<sub>v</sub>1 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 Ca<sub>v</sub>1 channels. |
topic |
neuromuscular junction neurotransmitter release acetylcholine nicotinic receptor calcium channel calcium transient |
url |
https://www.mdpi.com/1422-0067/22/16/9031 |
work_keys_str_mv |
AT nikitazhilyakov activationofneuronalnicotinicreceptorsinhibitsacetylcholinereleaseintheneuromuscularjunctionbyincreasingcasup2supfluxthroughcasubvsub1channels AT arseniiarkhipov activationofneuronalnicotinicreceptorsinhibitsacetylcholinereleaseintheneuromuscularjunctionbyincreasingcasup2supfluxthroughcasubvsub1channels AT artemmalomouzh activationofneuronalnicotinicreceptorsinhibitsacetylcholinereleaseintheneuromuscularjunctionbyincreasingcasup2supfluxthroughcasubvsub1channels AT dmitrysamigullin activationofneuronalnicotinicreceptorsinhibitsacetylcholinereleaseintheneuromuscularjunctionbyincreasingcasup2supfluxthroughcasubvsub1channels |
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