CaMKII Is Involved in the Choline-Induced Downregulation of Acetylcholine Release in Mouse Motor Synapses

Gaydukov, A. E.; Балезина, О. П.

doi:10.32607/20758251-2017-9-4-110-113

Cited by 4 publications

(3 citation statements)

References 10 publications

(14 reference statements)

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“…However, CaM-and CaMKII-dependent modulation of synaptic transmission resulted in different effects depending on distinct routes of calcium influx, patterns of synapse activation, and so on [39][40][41][42][43][44]. Recently, we have shown that in mouse NMJs, both spontaneous and evoked ACh release are insensitive to CaMKII blockers [44,45]. In addition, we previously identified the conditions under which CaMKII may be activated and oppositely modulate synaptic ACh release.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, we previously identified the conditions under which CaMKII may be activated and oppositely modulate synaptic ACh release. In particular, this occurs during selective activation of alpha7 nicotinic ACh receptors, when CaMKII mediates the inhibition of evoked ACh release [45]. It can also occur during the blockade of presynaptic phosphatase calcineurin, when the L-type VDCCs become disinhibited, leading to the activation of ryanodine receptors and CaMKII, which results in ACh release potentiation [44].…”

Section: Discussionmentioning

confidence: 99%

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Mechanism of P2X7 receptor-dependent enhancement of neuromuscular transmission in pannexin 1 knockout mice

Miteva

Gaydukov

Shestopalov

et al. 2018

Purinergic Signalling

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P2X7 receptors are present in presynaptic membranes of motor synapses, but their regulatory role in modulation of neurotransmitter release remains poorly understood. P2X7 receptors may interact with pannexin 1 channels to form a purinergic signaling unit. The potential mechanism of P2X7 receptor-dependent modulation of acetylcholine (ACh) release was investigated by recording miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) in neuromuscular junctions of wildtype (WT) and pannexin 1 knockout (Panx1 −/−) mice. Modulation of P2X7 receptors with the selective inhibitor A740003 or the selective agonist BzATP did not alter the parameters of either spontaneous or evoked ACh release in WT mice. In Panx1 −/− mice, BzATP-induced activation of P2X7 receptors resulted in a uniformly increased quantal content of EPPs during a short stimulation train. This effect was accompanied by an increase in the size of the readily releasable pool, while the release probability did not change. Inhibition of calmodulin by W-7 or of calcium/calmodulin-dependent kinase II (CaMKII) by KN-93 completely prevented the potentiating effect of BzATP on the EPP quantal content. The blockade of L-type calcium channels also prevented BzATP action on evoked synaptic activity. Thus, the activation of presynaptic P2X7 receptors in mice lacking pannexin 1 resulted in enhanced evoked ACh release. Such enhanced release was provoked by triggering the calmodulin-and CaMKIIdependent signaling pathway, followed by activation of presynaptic L-type calcium channels. We suggest that in WT mice, this pathway is downregulated due to pannexin 1-dependent tonic activation of inhibitory presynaptic purinergic receptors, which overcomes P2X7-mediated effects.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mechanism of P2X7 receptor-dependent enhancement of neuromuscular transmission in pannexin 1 knockout mice

Miteva

Gaydukov

Shestopalov

et al. 2018

Purinergic Signalling

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“…Experimental data ruled out the involvement of PLC and IP 3 receptor-mediated mechanisms [ 8 ], as well as the participation of atypical PKC isoforms [ 158 ] in the inhibitory role of α7 nAChR on neuromuscular transmission. This suggests that other effectors, like Ca 2+ /calmodulin-dependent protein kinase II and ryanodine receptors, may be involved instead [ 159 ].…”

Section: Perisynaptic Schwann Cells (Pscs): a Third-party Player In N...mentioning

confidence: 99%

Purinergic Tuning of the Tripartite Neuromuscular Synapse

2023

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The vertebrate neuromuscular junction (NMJ) is a specialised chemical synapse involved in the transmission of bioelectric signals between a motor neuron and a skeletal muscle fiber, leading to muscle contraction. Typically, the NMJ is a tripartite synapse comprising (a) a presynaptic region represented by the motor nerve ending, (b) a postsynaptic skeletal motor endplate area, and (c) perisynaptic Schwann cells (PSCs) that shield the motor nerve terminal. Increasing evidence points towards the role of PSCs in the maintenance and control of neuromuscular integrity, transmission, and plasticity. Acetylcholine (ACh) is the main neurotransmitter at the vertebrate skeletal NMJ, and its role is fine-tuned by co-released purinergic neuromodulators, like adenosine 5′-triphosphate (ATP) and its metabolite adenosine (ADO). Adenine nucleotides modulate transmitter release and expression of postsynaptic ACh receptors at motor synapses via the activation of P2Y and P2X receptors. Endogenously generated ADO modulates ACh release by acting via co-localised inhibitory A1 and facilitatory A2A receptors on motor nerve terminals, whose tonic activation depends on the neuronal firing pattern and their interplay with cholinergic receptors and neuropeptides. Thus, the concerted action of adenine nucleotides, ADO, and ACh/neuropeptide co-transmitters is paramount to adapting the neuromuscular transmission to the working load under pathological conditions, like Myasthenia gravis. Unravelling these functional complexities prompted us to review our knowledge about the way purines orchestrate neuromuscular transmission and plasticity in light of the tripartite synapse concept, emphasising the often-forgotten role of PSCs in this context.

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Cholinergic Modulation of Acetylcholine Secretion at the Neuromuscular Junction

Bukharaeva

Skorinkin

2021

J Evol Biochem Phys

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CaMKII Is Involved in the Choline-Induced Downregulation of Acetylcholine Release in Mouse Motor Synapses

Cited by 4 publications

References 10 publications

Mechanism of P2X7 receptor-dependent enhancement of neuromuscular transmission in pannexin 1 knockout mice

Mechanism of P2X7 receptor-dependent enhancement of neuromuscular transmission in pannexin 1 knockout mice

Purinergic Tuning of the Tripartite Neuromuscular Synapse

Cholinergic Modulation of Acetylcholine Secretion at the Neuromuscular Junction

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