Spontaneous Acetylcholine Release Potentiation Induced by 2-Arachidonoylglycerol and Anandamide in Mouse Motor Synapses

Tarasova, E. O.; Хоткина, Н. А.; Gaydukov, A. E.; Балезина, О. П.

doi:10.3103/s0096392521010053

Cited by 4 publications

(7 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this work, we made an attempt to reveal the mechanisms of the unusual potentiating effect of 2‐AG on ACh quantal size in mouse neuromuscular junctions previously described in our studies (Tarasova, Khotkina, Gaydukov, et al., 2021). There are currently only few reports about similar potentiating effects of cannabinoids in motor synapses (Morsch et al., 2018; Silveira et al., 2010).…”

Section: Discussionmentioning

confidence: 80%

“…During the second hour of incubation with 2‐AG, the amplitude of MEPP increased by 50% compared to control. This effect was prevented by an inverse agonist of CB1 receptors AM251 and by the vesicular ACh uptake inhibitor vesamicol (Tarasova, Khotkina, Gaydukov, et al., 2021), suggesting that the observed increase in quantal size is due to the presynaptic action of 2‐AG on CB1 receptors. The same potentiating effect of exogenous 2‐AG (1 μM) was reproduced in the present study (Figure 2, Table 1).…”

Section: Resultsmentioning

confidence: 99%

“…The specific and peculiar role of ECs in neuromuscular junctions gains great attention (Balezina et al., 2021; Behl et al., 2022; Dalle et al., 2022; Ge et al., 2020; Morsch et al., 2018; Tarasova, Khotkina, Gaydukov, et al., 2021) but still remains poorly studied up to date. Despite the relatively low density of CB1 receptors on muscle membranes, their activation by ECs plays a significant role in muscle metabolism and homeostasis (Alger, 2013; Charytoniuk et al., 2022; Dalle et al., 2022).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, we have found that in mouse neuromuscular synapses, the endocannabinoid (EC) 2‐arachidonylglycerol (2‐AG) is able to increase the amplitude of miniature endplate potentials (MEPPs) by acting on presynaptic cannabinoid CB1‐type receptors. This increase was prevented by vesamicol, an inhibitor of acetylcholine (ACh) uptake into synaptic vesicles (Tarasova, Khotkina, Bogacheva, et al., 2021; Tarasova, Khotkina, Gaydukov, et al., 2021).…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, latest research provides evidence that in mouse motor synapses, ECs can cause increase in MEPP amplitude and in the size of AСh quanta (Morsch et al., 2018; Tarasova, Khotkina, Gaydukov, et al., 2021; Gaydukov et al., 2020). This differs from the well‐known inhibitory effects of ECs on transmitter secretion in CNS synapses (Cristino et al., 2020; Ohno‐Shosaku & Kano, 2014).…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Quantal size increase induced by the endocannabinoid 2‐arachidonoylglycerol requires activation of CGRP receptors in mouse motor synapses

Tarasova,

Bogacheva,

Chernyshev

et al. 2023

Synapse

View full text Add to dashboard Cite

In mouse motor synapses, the exogenous application of the endocannabinoid (EC) 2‐arachidonoylglycerol (2‐AG) increases acetylcholine (ACh) quantal size due to the activation of CB1 receptors and the stimulation of ACh vesicular uptake. In the present study, microelectrode recordings of miniature endplate potentials (MEPP) revealed that this effect of 2‐AG is independent of brain‐derived neurotrophic factor (BDNF) signaling but involves the activation of calcitonin gene–related peptide (CGRP) receptors along with CB1 receptors. Potentiation of MEPP amplitude in the presence of 2‐AG was prevented by blockers of CGRP receptors and ryanodine receptors (RyR) and by inhibitors of phospholipase C (PLC) and Ca2+/calmodulin‐dependent protein kinase II (CaMKII). Therefore, we suggest a hypothetical chain of events, which starts from the activation of presynaptic CB1 receptors, involves PLC, RyR, and CaMKII, and results in CGRP release with the subsequent activation of presynaptic CGRP receptors. Activation of CGRP receptors is probably a part of a complex molecular cascade leading to the 2‐AG‐induced increase in ACh quantal size and MEPP amplitude. We propose that the same chain of events may also take place if 2‐AG is endogenously produced in mouse motor synapses, because the increase in MEPP amplitude that follows after prolonged tetanic muscle contractions (30 Hz, 2 min) was prevented by the blocking of CB1 receptors. This work may help to unveil the previously unknown aspects of the functional interaction between ECs and peptide modulators aimed at the regulation of quantal size and synaptic transmission.

show abstract

Section: Discussionmentioning

confidence: 80%

Section: Resultsmentioning

confidence: 99%