The Dogfish Neuromuscular Junction: Dual Innervation of Vertebrate Striated Muscle Fibres?

1972 ◽  
Vol 10 (3) ◽  
pp. 657-665
Author(s):  
Q. BONE
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Striated Muscle ◽  
Dense Core ◽  
The Other ◽  
Muscle Fibres ◽  
Nerve Terminals ◽  
Nerve Fibres ◽  
Different Types ◽  
Motor End Plate

In the myotomal muscles of the dogfish, Scyliorhinu canicula, there are 2 major types of fibre. The red fibres at the periphery of the myotome receive a distributed en grappe pattern of innervation. There are subjunctional folds at these endings, and the nerve terminals contain vesicles around 50 nm in diameter. In contrast to this, the white twitch fibres of the myotome are innervated focally, by 2 nerve fibres passing to the same motor end-plate. These 2 fibres contain vesicles of different types. One type of nerve terminal contains vesicles around 50 nm in diameter; these terminals resemble those upon the red fibres. The other contains vesicles up to 100 nm in diameter, frequently possessing a dense core. It is suggested that the white twitch fibres of dogfish are innervated by 2 separate axons, possibly containing different transmitter substances.

Distribution of acetylcholine receptors in the vicinity of nerve terminals on skeletal muscle of the frog

1972 ◽  
Vol 181 (1065) ◽  
pp. 431-440 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Connective Tissue ◽  
Neuromuscular Junction ◽  
Muscle Fibre ◽  
Nerve Terminal ◽  
Acetylcholine Receptors ◽  
Postsynaptic Membrane ◽  
Muscle Membrane ◽  
Muscle Fibres ◽  
Nerve Terminals

1. The acetylcholine (ACh) sensitivity of muscle fibres at the neuromuscular junction of the frog was investigated in preparations in which the nerve terminals could be clearly seen. 2. ACh released iontophoretically from a micropipette that was precisely positioned at various points along the muscle fibre in the vicinity of the synapse showed that the peak chemosensitivity (up to 1900 mV/nC) is confined to an area of postsynaptic membrane within a few micra of the nerve terminal; a tenfold decline in sensitivity was obtained when the ACh was released only 5 to 10 μm from the terminal’s edge. It is estimated that most of the response obtained when ACh is released within 40 μm from the terminal (the area covered in this study) is due to diffusion to the immediate postsynaptic area. The extrasynaptic chemosensitivity of the muscle membrane was too low to be measured with the present methods. 3. The accuracy with which micropipettes could be positioned in synaptic areas and the clarity of viewing nerve terminals were improved by bathing the tissue in collagenase, which reduced the amount of connective tissue. The distribution of chemosensitivity remained unchanged by such treatment. The ACh response was not detectably altered when nerve terminals were lifted off the muscle, exposing the subsynaptic muscle surface.

scholarly journals Simulating Reversibility of Dense Core Vesicles Capture in En Passant Boutons: Using Mathematical Modeling to Understand the Fate of Dense Core Vesicles in En Passant Boutons

2018 ◽  
Vol 140 (5) ◽  
Author(s):  
I. A. Kuznetsov ◽  
A. V. Kuznetsov
Keyword(s):  
Mathematical Modeling ◽  
Steady State ◽  
Nerve Terminal ◽  
Dense Core ◽  
Reasonable Assumption ◽  
Nerve Terminals ◽  
Dense Core Vesicles ◽  
Type Iii ◽  
Capture And Release ◽  
Kinetics Of

The goal of this paper is to use mathematical modeling to investigate the fate of dense core vesicles (DCVs) captured in en passant boutons located in nerve terminals. One possibility is that all DCVs captured in boutons are destroyed, another possibility is that captured DCVs can escape and reenter the pool of transiting DCVs that move through the boutons, and a third possibility is that some DCVs are destroyed in boutons, while some reenter the transiting pool. We developed a model by applying the conservation of DCVs in various compartments composing the terminal, to predict different scenarios that emerge from the above assumptions about the fate of DCVs captured in boutons. We simulated DCV transport in type Ib and type III terminals. The simulations demonstrate that, if no DCV destruction in boutons is assumed and all captured DCVs reenter the transiting pool, the DCV fluxes evolve to a uniform circulation in a type Ib terminal at steady-state and the DCV flux remains constant from bouton to bouton. Because at steady-state the amount of captured DCVs is equal to the amount of DCVs that reenter the transiting pool, no decay of DCV fluxes occurs. In a type III terminal at steady-state, the anterograde DCV fluxes decay from bouton to bouton, while retrograde fluxes increase. This is explained by a larger capture efficiency of anterogradely moving DCVs than of retrogradely moving DCVs in type III boutons, while the captured DCVs that reenter the transiting pool are assumed to be equally split between anterogradely and retrogradely moving components. At steady-state, the physiologically reasonable assumption of no DCV destruction in boutons results in the same number of DCVs entering and leaving a nerve terminal. Because published experimental results indicate no DCV circulation in type III terminals, modeling results suggest that DCV transport in these type III terminals may not be at steady-state. To better understand the kinetics of DCV capture and release, future experiments in type III terminals at different times after DCV release (molting) may be proposed.

Intraterminal Ca2+ and Spontaneous Transmitter Release at the Frog Neuromuscular Junction

2001 ◽  
Vol 85 (1) ◽  
pp. 287-294 ◽  
Author(s):  
J. K. Angleson ◽  
W. J. Betz
Keyword(s):  
Neuromuscular Junction ◽  
Phorbol Ester ◽  
Intracellular Recording ◽  
Transmitter Release ◽  
The Other ◽  
Nerve Terminals ◽  
Frog Neuromuscular Junction ◽  
Tetraacetic Acid ◽  
Ratiometric Imaging ◽  
The Relationship

We investigated the relationship between intraterminal Ca2+concentration ([Ca2+]i) and the frequency of miniature end plate potentials (MEPPs) at the frog neuromuscular junction by use of ratiometric imaging of fura-2-loaded nerve terminals and intracellular recording of MEPPs. Elevation of extracellular [KCl] over the range of 2–20 mM resulted in increases in [Ca2+]i and MEPP frequency. Loading terminals with the fast and slow Ca2+-buffers bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid-acetoxymethyl (BAPTA-AM) and EGTA-AM resulted in equivalent reductions in the KCl-dependent increases in MEPP frequency. The [Ca2+]i dependence of MEPP frequency determined by elevation of [Ca2+]i due to application of 0.1–10 μM ionomycin was similar to that determined when [Ca2+]i was raised by increasing extracellular KCl. Measurements in 10 mM extracellular KCl revealed that application of the phorbol ester phorbol 12 myristate 13-acetetate (PMA) caused an increase in MEPP frequency while the inactive analogue, 4α-PMA, did not. PMA application also caused an increase in [Ca2+]i. The relationship between [Ca2+]i and MEPP frequency in PMA was the same as was determined by the other methods of raising [Ca2+]i. Under all conditions tested, our data revealed a low [Ca2+]i threshold for activation of transmitter release and are consistent with a K d for [Ca2+]i on the order of 1 μM.

Spontaneous acetylcholine release in mammalian neuromuscular junctions

1997 ◽  
Vol 273 (6) ◽  
pp. C1835-C1841 ◽  
Author(s):  
Adriana Losavio ◽  
S. Muchnik
Keyword(s):  
Neuromuscular Junction ◽  
Acetylcholine Release ◽  
Neuromuscular Junctions ◽  
The Other ◽  
Nerve Terminals ◽  
Transmitter Secretion ◽  
Other Hand ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Lower Effect

Spontaneous secretion of the neurotransmitter acetylcholine in mammalian neuromuscular synapsis depends on the Ca2+ content of nerve terminals. The Ca2+ electrochemical gradient favors the entry of this cation. We investigated the possible involvement of three voltage-dependent Ca2+ channels (VDCC) (L-, N-, and P/Q-types) on spontaneous transmitter release at the rat neuromuscular junction. Miniature end-plate potential (MEPP) frequency was clearly reduced by 5 μM nifedipine, a blocker of the L-type VDCC, and to a lesser extent by the N-type VDCC blocker, ω-conotoxin GVIA (ω-CgTx, 5 μM). On the other hand, nifedipine and ω-CgTx had no effect on K+-induced transmitter secretion. ω-Agatoxin IVA (100 nM), a P/Q-type VDCC blocker, prevents acetylcholine release induced by K+ depolarization but failed to affect MEPP frequency in basal conditions. These results suggest that in the mammalian neuromuscular junction Ca2+ enters nerve terminals through at least three different channels, two of them (L- and N-types) mainly related to spontaneous acetylcholine release and the other (P/Q-type) mostly involved in depolarization-induced neurotransmitter release. Ca2+-binding molecule-related spontaneous release apparently binds Ca2+ very rapidly and would probably be located very close to Ca2+ channels, since the fast Ca2+ chelator (BAPTA-AM) significantly reduced MEPP frequency, whereas EGTA-AM, exhibiting slower kinetics, had a lower effect. The increase in MEPP frequency induced by exposing the preparation to hypertonic solutions was affected by neither external Ca2+concentration nor L-, N-, and P/Q-type VDCC blockers, indicating that extracellular Ca2+ is not necessary to produce hyperosmotic neurosecretion. On the other hand, MEPP frequency was diminished by BAPTA-AM and EGTA-AM to the same extent, supporting the view that hypertonic response is promoted by “bulk” intracellular Ca2+concentration increases.

scholarly journals On the supposed pluri-segmented innervation of muscle fibres

1925 ◽  
Vol 99 (694) ◽  
pp. 1-7 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Wallerian Degeneration ◽  
The Other ◽  
Muscle Fibres ◽  
Histological Findings ◽  
Spinal Segment ◽  
Mammalian Muscle ◽  
Motor End Plate ◽  
Skeletal Muscle Fibres ◽  
Segmental Innervation

Cattell and Stiles (1) have recently claimed to show that the majority of skeletal muscle fibres, at least in frogs, have a pluri-segmental innervation. The existence of a similar innervation in mammalian muscle fibres has also been asserted by Agdulhr (2). The evidence supporting this theory falls into two categories. The first is based on the histological findings after Wallerian degeneration has occurred in the axons rising from one spinal segment. In such cases muscle fibres were found in which one axon and motor end-plate showed signs of degeneration, and the other, when two were present, did not. Agduhr, who made the observation, concluded that the degenerated axon came from the segment whose motor roots he had cut 56 to 144 hours previously, and the undegenerated axon from another spinal segment. He was careful, however, to point out in his last paper that the total number of such doubly (or trebly) innervated fibres could not be adduced from his experiments.

Acetylcholine receptors at the rat neuromuscular junction as revealed by deep etching

1982 ◽  
Vol 215 (1199) ◽  
pp. 147-154 ◽  
Keyword(s):  
Neuromuscular Junction ◽  
Basal Lamina ◽  
Acetylcholine Receptors ◽  
Postsynaptic Membrane ◽  
Muscle Fibres ◽  
Nerve Terminals ◽  
Single Muscle ◽  
Deep Etching ◽  
Collagenase Treatment ◽  
Regular Arrangement

Collagenase treatment of rat intercostal muscles yielded single muscle fibres in which the nerve terminals and basal lamina were removed allowing an unimpeded view of the ecternal surface of the postsynaptic membrane. This was revealed by deep etching of freeze-fractured preparations and appeared as a maze of folds separated by deep troughs, showing on the crests of the folds a densely packed population of protrusions about 8⋅5 nm in diameter. These densely packed protrusions ( ca . 9000 μm -2 ) are mainly confined to the postsynaptic regions of the sarcolemma and presumably represent the acetycholine receptor molecules, which are highly concenrated in these areas. The protrusions are generally tightly packed without obvious regular arrangement, but in some areas, usually on the tops of the crests, they are arranged into irregular rows normal to the long axis of the folds.

Steroid anaesthetics: inhibition of depolarization–secretion coupling at the mouse motor nerve terminal

1980 ◽  
Vol 58 (10) ◽  
pp. 1221-1228 ◽  
Author(s):  
P. Pennefather ◽  
E. Puil ◽  
D. M. J. Quastel
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Motor Nerve ◽  
Motor Nerve Terminal ◽  
Nerve Terminals ◽  
Potassium Depolarization ◽  
End Plate

The coupling between nerve terminal depolarization and quantal secretion of acetylcholine at the mouse neuromuscular junction was estimated by measuring the multiplication of the frequency of miniature end-plate potentials (m.e.p.p.s) produced by increasing the concentration of calcium in the medium from 0.1 to 1.0 mM in the presence of 15 mM potassium. Depolarization–secretion coupling was inhibited by the anaesthetic steroids progesterone, pregnanedione, and alphaxalone. The nonanaesthetic steroid Δ16-alphaxalone also inhibited depolarization–secretion coupling with the same potency as alphaxalone. This result indicates that inhibition of depolarization–secretion coupling in nerve terminals is unlikely to play a major role in the production of anaesthesia.

A Histological Study of the Peripheral Receptors in the Thorax of Land Isopods, with Special Reference to the Location of Possible Hygroreceptors

1963 ◽  
Vol s3-104 (67) ◽  
pp. 337-350
Author(s):  
D. E. JANS ◽  
K. F. A. ROSS
Keyword(s):  
Special Reference ◽  
Histological Study ◽  
The Body ◽  
The Other ◽  
Serial Sections ◽  
Nerve Fibres ◽  
Porcellio Scaber ◽  
Different Types ◽  
Thoracic And Abdominal ◽  
Lateral Plates

By double embedding whole isopods in paraffin wax and celloidin, after fixing them in Bodian's fluid, it was possible to obtain complete sets of undamaged serial sections through the thoracic and abdominal regions of females of Oniscus asellus L. and Porcellio scaber Latr., and also some incomplete series through males of these species and a species of the genus Armadillidium. These sections were stained by the methods of Bodian and of Holmes to show the nerve-fibres. They were then carefully studied, and the distribution and the morphology of all peripheral nerveendings and receptors in the body were determined as completely as possible. In all, 6 different types of terminations were found; and in some cases it was possible to draw valid inferences about their probable function from a consideration of their location and their morphology alone. Three of them are probably tactile. The function of the other three is much more uncertain; but one of them, a group of pit-like terminations situated on the under side of the lateral plates on each side of the thoracic segments, is particularly suitably located to function as a receptor of temperature or humidity, and morphologically it bears some resemblance to certain proven hygroreceptors in other arthropods. This particular termination and one of the other types, consisting of ventrally situated partially retracted hairs, do not appear to have been described previously in the land isopods.

Effects of adenosine on Ca2+ entry in the nerve terminal of the frog neuromuscular junction

1999 ◽  
Vol 77 (9) ◽  
pp. 707-714 ◽  
Author(s):  
Richard Robitaille ◽  
Sébastien Thomas ◽  
Milton P Charlton
Keyword(s):  
Neuromuscular Junction ◽  
Nerve Terminal ◽  
Nerve Stimulation ◽  
High Frequency ◽  
Transmitter Release ◽  
Synaptic Depression ◽  
Presynaptic Terminal ◽  
Nerve Terminals ◽  
Frog Neuromuscular Junction ◽  
Induced Changes

This study aimed to test whether nerve-evoked and adenosine-induced synaptic depression are due to reduction in Ca2+ entry in nerve terminals of the frog neuromuscular junction. Nerve terminals were loaded with the fluorescent Ca2+ indicator fluo 3 (fluo 3-AM) or loaded with dextran-coupled Ca2+ green-1 transported from the cut end of the nerve. Adenosine (10-50 µM) did not change the resting level of Ca2+ in the presynaptic terminal, whereas it induced large Ca2+ responses in perisynaptic Schwann cells, indicating that adenosine was active and might have induced changes in the level of Ca2+ in the nerve terminal. Ca2+ responses in nerve terminals could be induced by nerve stimulation (0.5 or 100 Hz for 100 ms) over several hours. In the presence of adenosine (10 µM), the size and duration of the nerve-evoked Ca2+ responses were unchanged. When extracellular Ca2+ concentration was lowered to produce the same reduction in transmitter release as the application of adenosine, Ca2+ responses induced by nerve stimulations were reduced by 40%. This indicates that changes in Ca2+ responsible for the decrease in release should have been detected if the mechanism of adenosine depression involved partial block of Ca2+ influx. Ca2+ responses evoked by prolonged high frequency trains of stimuli (50 Hz for 10 or 30 s), which caused profound depression of transmitter release, were sustained during the whole duration of the stimulation, and adenosine had no effect on these responses. These data indicate that neither adenosine induced synaptic depression nor stimulation-induced synaptic depression are caused by reductions in Ca2+ entry into the presynaptic terminal in the frog neuromuscular junction.Key words: adenosine, Ca2+, nerve terminal, transmitter release, synaptic depression.

Effects of high calcium solutions on glutamate sensitivity of crayfish muscle fibres

1980 ◽  
Vol 209 (1176) ◽  
pp. 415-429 ◽  
Keyword(s):  
Nerve Terminal ◽  
Aminobutyric Acid ◽  
Inhibitory Synapses ◽  
Muscle Fibres ◽  
Nerve Terminals ◽  
Direct Stimulation ◽  
Calcium Spikes ◽  
Crayfish Muscle ◽  
High Calcium ◽  
Denervated Muscles

Crayfish neuromuscular preparations were studied after 18-36 h exposure to high calcium solutions. As previously reported for frog neuromuscular preparations the treatment damaged the nerve terminals and decreased junctional potentials. The resting potentials and input resistances of the muscle fibres were not affected; but their sensitivity to glutamate was significantly decreased when compared to that of control muscles. After exposure to high calcium, the sensitivity to γ-aminobutyric acid, the putative transmitter at inhibitory synapses, was increased. Apparently normal twitches were elicited by direct stimulation, and calcium spikes could still be observed in the fibres. A decreased sensitivity to glutamate was also noted in experiments carried out on denervated muscles 8 months after section of the motor axons. Possible relations between nerve terminal damage and the decrease in sensitivity to glutamate are discussed.

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