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Volume 22
Issue 16
10.3390/ijms22169031
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Article

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

by
Nikita Zhilyakov
1,*,
Arsenii Arkhipov
1,
Artem Malomouzh
1 and
Dmitry Samigullin
1,2,*
1
Kazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center, Russian Academy of Sciences, P.O. Box 261, 420111 Kazan, Russia
2
Department of Radiophotonics and Microwave Technologies, Federal State Budgetary Educational Institution of Higher Education “Kazan National Research Technical University Named after A.N. Tupolev–KAI”, 420111 Kazan, Russia
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2021, 22(16), 9031; https://doi.org/10.3390/ijms22169031
Submission received: 10 August 2021 / Revised: 18 August 2021 / Accepted: 19 August 2021 / Published: 21 August 2021
(This article belongs to the Special Issue Light-Controlled Modulation and Analysis of Neuronal Functions)
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Abstract

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.
Keywords: neuromuscular junction; neurotransmitter release; acetylcholine; nicotinic receptor; calcium channel; calcium transient neuromuscular junction; neurotransmitter release; acetylcholine; nicotinic receptor; calcium channel; calcium transient

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MDPI and ACS Style

Zhilyakov, N.; Arkhipov, A.; Malomouzh, A.; Samigullin, D. Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca2+ Flux through Cav1 Channels. Int. J. Mol. Sci. 2021, 22, 9031. https://doi.org/10.3390/ijms22169031

AMA Style

Zhilyakov N, Arkhipov A, Malomouzh A, Samigullin D. Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca2+ Flux through Cav1 Channels. International Journal of Molecular Sciences. 2021; 22(16):9031. https://doi.org/10.3390/ijms22169031

Chicago/Turabian Style

Zhilyakov, Nikita, Arsenii Arkhipov, Artem Malomouzh, and Dmitry Samigullin. 2021. "Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca2+ Flux through Cav1 Channels" International Journal of Molecular Sciences 22, no. 16: 9031. https://doi.org/10.3390/ijms22169031

APA Style

Zhilyakov, N., Arkhipov, A., Malomouzh, A., & Samigullin, D. (2021). Activation of Neuronal Nicotinic Receptors Inhibits Acetylcholine Release in the Neuromuscular Junction by Increasing Ca2+ Flux through Cav1 Channels. International Journal of Molecular Sciences, 22(16), 9031. https://doi.org/10.3390/ijms22169031

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