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

Tsentsevitsky, A. N.; Kovyazina, I. V.; Нуруллин, Л. Ф.; Nikolsky, E. E.

doi:10.1016/j.neulet.2017.04.015

Cited by 12 publications

(22 citation statements)

References 28 publications

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“…Drug was injected in a 1 ml volume over a 10 min period under the control of a syringe pump (Stoelting) while the animal was freely behaving during electrophysiological recording. Atropine sulfate (0.5, 2.5, 5, and 10 mg; Honda et al, 2004) Bader and Diener, 2015; Tsentsevitsky et al, 2017), and tropicamide (2, 4, and 8 mg; Lazareno et al, 1990;Hernández et al, 1993;Veeraragavan et al, 2011) were administered respectively in different groups. The injection cannula was left in place until the recording ended.…”

Section: Intraperitoneal Injection and Microinjectionmentioning

confidence: 99%

The Firing of Theta State-Related Septal Cholinergic Neurons Disrupt Hippocampal Ripple Oscillations via Muscarinic Receptors

Zhang

Wang

et al. 2020

J. Neurosci.

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The septo-hippocampal cholinergic system is critical for hippocampal learning and memory. However, a quantitative description of the in vivo firing patterns and physiological function of medial septal (MS) cholinergic neurons is still missing. In this study, we combined optogenetics with multichannel in vivo recording and recorded MS cholinergic neuron firings in freely behaving male mice for 5.5-72 h. We found that their firing activities were highly correlated with hippocampal theta states. MS cholinergic neurons were highly active during theta-dominant epochs, such as active exploration and rapid eye movement sleep, but almost silent during nontheta epochs, such as slow-wave sleep (SWS). Interestingly, optogenetic activation of these MS cholinergic neurons during SWS suppressed CA1 ripple oscillations. This suppression could be rescued by muscarinic M 2 or M 4 receptor antagonists. These results suggest the following important physiological function of MS cholinergic neurons: maintaining high hippocampal acetylcholine level by persistent firing during theta epochs, consequently suppressing ripples and allowing theta oscillations to dominate.

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Section: Intraperitoneal Injection and Microinjectionmentioning

confidence: 99%

The Firing of Theta State-Related Septal Cholinergic Neurons Disrupt Hippocampal Ripple Oscillations via Muscarinic Receptors

Zhang

Wang

et al. 2020

J. Neurosci.

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“…Santafe et al revealed the immunoexpression of all five (M1-M5) currently identified mAChR subtypes in the rat neuromuscular junction [ 32 , 33 ]. Tsentsevitsky et al then identified all these subtypes of mAChRs at the motor-nerve terminals of frog cutaneous pectoris muscle [ 41 ]. The diversity of mAChRs could be one of the reasons for dependence on the observed effects of their modulation on the experimental conditions and might explain the contradictory data on the participation of different mAChRs in the regulation of synaptic transmission.…”

Section: Presynaptic Acetylcholine Receptors Modulate the Kinetics Of...mentioning

confidence: 99%

“…Activation of mAChRs by muscarine, which is an agonist for all mAChRs, induced the shortening distribution of “real” synaptic delays of EPCs recorded in a low Ca 2+ /high Mg 2+ solution at the frog neuromuscular junction. Selective antagonists of M1, M2, and M4 mAChRs have prevented the synchronizing action of muscarine on ACh secretion [ 41 ].…”

Section: Presynaptic Acetylcholine Receptors Modulate the Kinetics Of...mentioning

confidence: 99%

“…At a later date, it was shown that muscarine decreased the quantal content of the multiquantal EPCs and synchronized the quanta secretion [ 41 ]. The depressing action of muscarine on the EPC quantal content was abolished by pretreatment with the specific blockers of muscarinic receptors, namely 4-DAMP and J 104129 ( Table 1 ).…”

Section: Presynaptic Acetylcholine Receptors Modulate the Kinetics Of...mentioning

confidence: 99%

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Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions

et al. 2022

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For effective transmission of excitation in neuromuscular junctions, the postsynaptic response amplitude must exceed a critical level of depolarization to trigger action potential spreading along the muscle-fiber membrane. At the presynaptic level, the end-plate potential amplitude depends not only on the acetylcholine quanta number released from the nerve terminals in response to the nerve impulse but also on a degree of synchronicity of quanta releases. The time course of stimulus-phasic synchronous quanta secretion is modulated by many extra- and intracellular factors. One of the pathways to regulate the neurosecretion kinetics of acetylcholine quanta is an activation of presynaptic autoreceptors. This review discusses the contribution of acetylcholine presynaptic receptors to the control of the kinetics of evoked acetylcholine release from nerve terminals at the neuromuscular junctions. The timing characteristics of neurotransmitter release is nowadays considered an essential factor determining the plasticity and efficacy of synaptic transmission.

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“…Since the midst of the 20th century, the data began to accumulate indicating that ACh, released in the synaptic cleft from the nerve endings, activates presynaptic cholinergic receptors, thus exerting a modulatory effect on the neurotransmission process by changing the amount and/or dynamics of subsequent portions of neurotransmitter release [2][3][4][5][6][7]. Initially pharmacologically, and later by other methods it has been shown that both ionotropic nicotinic and metabotropic muscarinic cholinergic receptors are present in the motor nerve terminal, and the activation of these receptors can lead to autoregulation of ACh release [4,5,[8][9][10][11]. According to the data of morphological and functional analysis, presynaptic cholinergic receptors can be located both near the active zones and relatively far from the synaptic cleft [4,12,13].…”

Section: Introductionmentioning

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

IJMS

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

Cited by 12 publications

References 28 publications

The Firing of Theta State-Related Septal Cholinergic Neurons Disrupt Hippocampal Ripple Oscillations via Muscarinic Receptors

The Firing of Theta State-Related Septal Cholinergic Neurons Disrupt Hippocampal Ripple Oscillations via Muscarinic Receptors

Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions

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

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