Cholinergic regulation of the evoked quantal release at frog neuromuscular junction

Nikolsky, E. E.; Vyskočil, F.; Bukharaeva, É. A.; Samigullin, Dmitry; Lg, Magazanik

doi:10.1113/jphysiol.2004.065805

Cited by 43 publications

(37 citation statements)

References 63 publications

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“…The potency of nicotine and other cholinergic agonists to inhibit Ach release during rhythmic activity in the peripheral synapses was previously observed during their short-term (1-3 min) application at high (micromolar and higher) concentrations [12,13]. It was hypothesized that this inhibitory action is mediated via activation of presynaptic neuronaltype nChR.…”

Section: Resultsmentioning

confidence: 94%

Effect of nicotine on neuromuscular transmission in mouse motor synapses

2006

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Section: Resultsmentioning

confidence: 94%

Effect of nicotine on neuromuscular transmission in mouse motor synapses

2006

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“…Neurotransmitter release from frog nerve endings is modulated by cholinomimetics: by acting through nicotinic receptors, they change kinetics of secretion and its quantum content, while by activation of muscarinic receptors they contribute only to regulation of quantum content (Ciani and Edwards, 1963; Nikolsky et al, 2004). Both quantum content and kinetics of neurotransmitter secretion directly depend on the level of [Ca 2+ ] i in presynaptic terminal (Katz and Miledi, 1965; Nikol'skiĭ et al, 2000; Samigullin et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Although this phenomenon has received a significant research attention in the past (Nikol'skiĭ and Giniatullin, 1979; Wessler, 1989; Macleod et al, 1994; Van der Kloot et al, 1997; Nikolsky et al, 2004), fine details of ACh-dependent presynaptic regulation remain obscure. Both direct action of ACh on exocytotic machinery (Linial et al, 1997) and inhibition of presynaptic Ca 2+ entry (Wu and Saggau, 1997; Parnas et al, 2000; Khaziev et al, 2012) have been suggested.…”

Section: Introductionmentioning

confidence: 99%

Acetylcholine-Induced Inhibition of Presynaptic Calcium Signals and Transmitter Release in the Frog Neuromuscular Junction

et al. 2016

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Acetylcholine (ACh), released from axonal terminals of motor neurons in neuromuscular junctions regulates the efficacy of neurotransmission through activation of presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated presynaptic regulation could reflect either direct action on exocytotic machinery or modulation of Ca2+ entry and resulting intra-terminal Ca2+ dynamics. We have measured free intra-terminal cytosolic Ca2+ ([Ca2+]i) using Oregon-Green 488 microfluorimetry, in parallel with voltage-clamp recordings of spontaneous (mEPC) and evoked (EPC) postsynaptic currents in post-junctional skeletal muscle fiber. Activation of presynaptic muscarinic and nicotinic receptors with exogenous acetylcholine and its non-hydrolized analog carbachol reduced amplitude of the intra-terminal [Ca2+]i transients and decreased quantal content (calculated by dividing the area under EPC curve by the area under mEPC curve). Pharmacological analysis revealed the role of muscarinic receptors of M2 subtype as well as d-tubocurarine-sensitive nicotinic receptor in presynaptic modulation of [Ca2+]i transients. Modulation of synaptic transmission efficacy by ACh receptors was completely eliminated by pharmacological inhibition of N-type Ca2+ channels. We conclude that ACh receptor-mediated reduction of Ca2+ entry into the nerve terminal through N-type Ca2+ channels represents one of possible mechanism of presynaptic modulation in frog neuromuscular junction.

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“…250-400 single quantal postsynaptic responses and nerve ending currents were recorded; they were digitized with a sampling rate of 5 μs and analyzed using a software developed in our laboratory. In addition to the quantal content of EPCs, the degree of the neurotransmitter quanta release synchrony in response to electrical stimuli was evaluated by analyz ing the variance of true synaptic delays (the interval from peak of the sodium component of the nerve end ing current to the beginning of the EPC at the 20% level of its maximal amplitude) [12]. For this purpose, distribution histograms and cumulative curves of synap tic delays were plotted.…”

Section: Revealing Of T Type Low Voltage Activated Calcium Channels (mentioning

confidence: 99%

“…For this purpose, distribution histograms and cumulative curves of synap tic delays were plotted. Cumulative curves were used to estimate the parameter Р 90 (the interval where 90% of all synaptic delays fell), which characterizes the syn chrony of the neurotransmitter quantum release [12]. In addition to the neurotransmitter release rate, amplitude and time parameters of EPCs were analyzed.…”

Section: Revealing Of T Type Low Voltage Activated Calcium Channels (mentioning

confidence: 99%

Revealing of T-type low-voltage activated calcium channels (CaV3) in frog neuromuscular junctions

et al. 2013

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Increase in the intracellular level of Ca 2+ concen tration leads to the initiation of a wide range of mole cular processes, including the activation of Ca 2+ dependent enzymes, gene expression, neurotransmit ter release, etc.[1]. In spite of the variety of channels and pumps involved in the regulation of the intracellu lar Ca 2+ metabolism, the main role in Ca 2+ signaling is attributed to voltage activated Ca 2+ channels [2]. According to the modern classification based on the structural features of the pore forming subunit α 1 , all voltage activated Ca 2+ channels (Ca V ) are divided into three families. The first family (Ca V 1.1, Ca V 1.2, Ca V 1.3, Ca V 1.4) includes high voltage activated chan nels containing the subunits α 1S , α 1C , α 1D , α 1F , respectively, which mediate L type Ca 2+ currents. The second family (Ca V 2.1, Ca V 2.2, Ca V 2.3) includes high voltage activated channels with subunits α 1A , α 1B , α 1E , respectively, which mediate the P/Q , N , and R types of Ca 2+ currents. The third family (Ca V 3.1, Ca V 3.2, Ca V 3.3) includes low voltage activated channels with subunits α 1G , α 1H , α 1I , respectively, which mediate T type Ca 2+ channels [1].

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Cholinergic regulation of the evoked quantal release at frog neuromuscular junction

Cited by 43 publications

References 63 publications

Effect of nicotine on neuromuscular transmission in mouse motor synapses

Effect of nicotine on neuromuscular transmission in mouse motor synapses

Acetylcholine-Induced Inhibition of Presynaptic Calcium Signals and Transmitter Release in the Frog Neuromuscular Junction

Revealing of T-type low-voltage activated calcium channels (CaV3) in frog neuromuscular junctions

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