Quantal acetylcholine release at the vertebrate neuromuscular junction.

Kloot, William Van der; Molgó, Jordi

doi:10.1152/physrev.1994.74.4.899

Cited by 246 publications

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“…It is known that the release of acetylcholine from motor nerve terminals can also be modulated by endogenous agents other than acetylcholine, such as adenosine, catecholamines, metabolic arachidonic acid, calcitonin gene-related peptide, substance P, VIP, and hormones (16,17). Thus, the present study shows that NO may possibly represent another modulating factor of acetylcholine release by the motor nerve terminal.…”

supporting

confidence: 52%

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Queiroz

Alves-Do-Prado

2001

Braz J Med Biol Res

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In rats, the nitric oxide (NO)-synthase pathway is present in skeletal muscle, vascular smooth muscle, and motor nerve terminals. Effects of NO were previously studied in rat neuromuscular preparations receiving low (0.2 Hz) or high (200 Hz) frequencies of stimulation. The latter frequency has always induced tetanic fade. However, in these previous studies we did not determine whether NO facilitates or impairs the neuromuscular transmission in preparations indirectly stimulated at frequencies which facilitate neuromuscular transmission. Thus, the present study was carried out to examine the effects of NO in rat neuromuscular preparations indirectly stimulated at 5 and 50 Hz. The amplitude of muscular contraction observed at the end (B) of a 10-s stimulation was taken as the ratio (R) of that obtained at the start (A) (R = B/A). S-nitroso-N-acetylpenicillamine (200 µM), superoxide dismutase (78 U/ml) and L-arginine (4.7 mM), but not D-arginine (4.7-9.4 mM), produced an increase in R (facilitation of neurotransmission) at 5 Hz. However, reduction in the R value (fade of transmission) was observed at 50 Hz. N G -nitro-L-arginine (8.0 mM) antagonized both the facilitatory and inhibitory effects of L-arginine (4.7 mM). The results suggest that NO may modulate the release of acetylcholine by motor nerve terminals. Key words Nitric oxide (NO) is synthesized by NOsynthase (NOS) (1-3). In the rat, NOS is present in the sarcolemma of type II fibers of skeletal muscle (4), in vascular smooth muscle (5), and in motor nerve terminals (6). Since NOS is a stereospecific enzyme, the effects induced by L-arginine are not observed in the presence of D-arginine under similar experimental conditions (7,8)L-arginine methyl ester; L-arginine ethyl ester, and N G -nitro-L-arginine methyl ester) are used as inhibitors of NOS. The effects produced by endogenous NO (from L-arginine) are pharmacologically similar to those induced by NO released from an exogenous source such as 3-(4-morpholinyl)-syndonone imine (SIN-1) or S-nitroso-N-acetylpenicillamine (SNAP) (9).The amplitude of muscular contraction (AMC) is stable when the diaphragm is indirectly stimulated at 0.2 Hz. A progressive increase in AMC is observed at 5 Hz (see Acting at the presynaptic level, the NO precursor L-arginine (4.7-9.4 mM) produces a dose-dependent increase of AMC in rat neuromuscular preparations indirectly stimulated at 0.2 Hz (10). In contrast, acting on skeletal muscle, it reduces AMC in preparations previously paralyzed with d-tubocurarine and directly stimulated at 0.2 Hz (10). The presynaptic action of NO reduces the effect produced by its postsynaptic action (10). On the other hand, the NO precursor Larginine (4.7 to 9.4 mM) or SIN-1 acting at the presynaptic level produces a dose-dependent increase in tetanic fade when the nerve is stimulated at 200 Hz (11). The same high frequency of stimulation reduces the maximal tetanic tension (postsynaptic action) when applied to the rat phrenic nerve diaphragm preparation previously treated with L-arginine o...

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confidence: 52%

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Queiroz

Alves-Do-Prado

2001

Braz J Med Biol Res

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“…It rapidly hydrolyzes acetylcholine released from the nerve terminals [30]. It is well established that AChE activity is also influenced by the pattern of nerve impulses, muscle electromechanical activity and neurogenic substances conveyed by axonal transport [31].…”

Section: The Morphometric Resultsmentioning

confidence: 99%

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Mokhmer¹,

Saber²,

Hamouda³

et al. 2017

J Cytol Histol

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“…A suitable candidate is the Ca¥-binding protein synaptotagmin III which, in contrast to synaptotagmin I, has high Ca¥ affinity and functions in the presence of Sr¥ as well as Ca¥ (for review see Geppert & S udhof, 1998). A more traditional explanation is the 'residual ion' model (Dodge et al 1969;Bain & Quastel, 1992;van der Kloot & Molg o, 1993) in which the asynchronous phase is due to Sr¥ accumulating temporarily in the presynaptic terminal (for review see van der Kloot & Molg o, 1994). A mainstay of this hypothesis regarding late release mediated by Sr¥ influx was that, as shown here for central inhibitory synapses, BAPTA AM curtailed Sr¥-induced late release.…”

Section: Discussionmentioning

confidence: 99%

Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Rumpel

Behrends

1999

The Journal of Physiology

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In all preparations studied, a characteristic distinction of Sr¥versus Ca¥-mediated synaptic transmission is a reduced early (or phasic) component and an augmented late (or asynchronous) tail of individual miniature-like events called 'late release'. Thus, transmission in Sr¥ is desynchronized with respect to the normal situation. Understanding this non-physiological phenomenon may entail important insights into the mechanisms which under physiological conditions control the kinetics of evoked transmitter release. Thus, have proposed that preferential activation by Sr¥ of late, asynchronous release is due to binding at a secondary, highaffinity divalent cation binding site, where the action of Sr¥ is stronger than that of Ca¥. A high-affinity site in addition to the putative low-affinity receptor involved in synchronous release (cf. Heidelberger et al. 1994) has also been postulated in order to account for use-dependent synaptic facilitation (Yamada & Zucker, 1992). The twobinding-site hypothesis has gained indirect support from experiments on excitatory synapses lacking the presynaptic Ca¥-binding protein synaptotagmin I, where phasic release was suppressed and asynchronous release was intact or increased (Geppert et al. 1994). Alternatively, it has been suggested that a single releaseinducing binding site may suffice to explain Sr¥-induced late release if buffering, extrusion or sequestration are assumed to be less efficient for Sr¥ than for Ca¥ so that free Sr¥ concentration remains elevated for longer times

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Quantal acetylcholine release at the vertebrate neuromuscular junction.

Cited by 246 publications

References 0 publications

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

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Quantal acetylcholine release at the vertebrate neuromuscular junction.

Cited by 246 publications

References 0 publications

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Structural Changes in the Skeletal Muscle Fiber of Adult Male Albino Rat Following Atorvastatin Treatment; the Possible Mechanisms of Atorvastatin Induced Myotoxicity

Sr2+‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

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Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro