Degenerative changes in the function of neuromuscular junctions of Manduca sexta during metamorphosis

1992 ◽  
Vol 167 (1) ◽  
pp. 61-89
Author(s):  
I. M. Sonea ◽  
M. B. Rheuben
Keyword(s):  
Manduca Sexta ◽  
Muscle Fiber ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Normal Function ◽  
Degenerative Changes ◽  
Resting Potential ◽  
Morphological Evidence ◽  
Low Frequencies ◽  
Cable Properties

In Manduca sexta the decline in neuromuscular function during metamorphic degeneration was compared in two muscles which differed characteristically with regard to pre- and postsynaptic physiological properties. In both muscles, morphological evidence indicated that a significant number of the active zones within the population of neuromuscular junctions on a given fiber were nonfunctional. Nevertheless, the degenerating nerve terminals were able to produce an above-threshold excitatory junction potential (EJP) which was facilitated in a manner characteristic of the muscle being observed. Abnormal findings during the early stages of degeneration included a larger than normal EJP, a decline in EJP amplitude over a 20 min period even with low frequencies of stimulation, an increase in EJP duration, a decline in muscle fiber resting potential amplitude with age, a decrease or disappearance of post-tetanic potentiation and long-term facilitation, and an increased likelihood that the motor nerve would fail to conduct a stimulus. The two muscles were qualitatively similar but quantitatively different with regard to these degenerative changes. It is suggested that this combination of relatively normal function with abnormal properties might be associated with the withdrawal of glial processes from the neuromuscular junctions, changes in the cable properties associated with shrivelling of the muscle fibers, and a decline in the metabolic functions supporting both muscle fiber resting potentials and those underlying transmitter synthesis, mobilization and release.

scholarly journals Degenerative changes in the structure of neuromuscular junctions of Manduca sexta during metamorphosis

1992 ◽  
Vol 167 (1) ◽  
pp. 119-154
Author(s):  
M. B. Rheuben
Keyword(s):  
Manduca Sexta ◽  
Muscle Fiber ◽  
Nerve Terminal ◽  
Structural Changes ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Freeze Fracture ◽  
Outer Region ◽  
Peripheral Region ◽  
Phagocytic Cells

During the degenerative processes that precede and accompany metamorphosis of the larval mesothoracic dorsal longitudinal muscles of Manduca sexta, the motor nerves and neuromuscular junctions undergo a variety of structural changes that are largely secondary to the changing morphologies of their respective glia. In the central region of the main motor nerve, the multiple layers of glial processes surrounding each of the large axons withdraw, leaving them apposed. In the peripheral region of the main motor nerve and in the secondary and tertiary nerve branches supplying the muscle, the outer glial processes of the nerve sheath and those that loosely wrap accompanying small neurosecretory axons all swell. Phagocytic cells and cells of unknown function invade the outer region of the nerve. In the neuromuscular junctions, the glial cells withdraw their processes from a complicated interdigitation with processes from the muscle fiber and from their relationship with the nerve terminal. As degeneration proceeds, this allows a greater area of contact between each nerve terminal and the muscle fiber. Within each junction there is a mixture of both functional and non-functional regions and active zones, as determined by both thin-section and freeze-fracture observations. No correlation was found between the degree of degeneration of a neuromuscular junction and its association with a particular muscle fiber or its position on the fiber relative to the origin or insertion.

scholarly journals Glutamate at the Vertebrate Neuromuscular Junction: From Modulation to Neurotransmission

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 996 ◽  
Author(s):  
Colombo ◽  
Francolini
Keyword(s):  
Neuromuscular Junction ◽  
Signaling Pathways ◽  
Muscle Fiber ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Vertebrate Development ◽  
Motor Nerve Ending ◽  
Downstream Signaling ◽  
Synaptic Neurotransmission ◽  
Synaptic Receptors

Although acetylcholine is the major neurotransmitter operating at the skeletal neuromuscular junction of many invertebrates and of vertebrates, glutamate participates in modulating cholinergic transmission and plastic changes in the last. Presynaptic terminals of neuromuscular junctions contain and release glutamate that contribute to the regulation of synaptic neurotransmission through its interaction with pre- and post-synaptic receptors activating downstream signaling pathways that tune synaptic efficacy and plasticity. During vertebrate development, the chemical nature of the neurotransmitter at the vertebrate neuromuscular junction can be experimentally shifted from acetylcholine to other mediators (including glutamate) through the modulation of calcium dynamics in motoneurons and, when the neurotransmitter changes, the muscle fiber expresses and assembles new receptors to match the nature of the new mediator. Finally, in adult rodents, by diverting descending spinal glutamatergic axons to a denervated muscle, a functional reinnervation can be achieved with the formation of new neuromuscular junctions that use glutamate as neurotransmitter and express ionotropic glutamate receptors and other markers of central glutamatergic synapses. Here, we summarize the past and recent experimental evidences in support of a role of glutamate as a mediator at the synapse between the motor nerve ending and the skeletal muscle fiber, focusing on the molecules and signaling pathways that are present and activated by glutamate at the vertebrate neuromuscular junction.

Degenerative changes in the muscle fibers of Manduca sexta during metamorphosis

1992 ◽  
Vol 167 (1) ◽  
pp. 91-117 ◽  
Author(s):  
M. B. Rheuben
Keyword(s):  
Manduca Sexta ◽  
Basal Lamina ◽  
Muscle Fiber ◽  
Structural Changes ◽  
Muscle Fibers ◽  
Resting Potential ◽  
Ultrastructural Changes ◽  
Intimate Contact ◽  
Cross Sectional ◽  
Dense Granules

The ultrastructural changes associated with the early stages of degeneration of the larval mesothoracic muscle fibers of Manduca sexta were examined during the prepupal period and on the first day after ecdysis. Over this 5 day period, the muscle fibers decrease in cross-sectional area but increase in apparent surface area compared to the dimensions of early fifth-instar fibers. Large numbers of electron-dense granules or droplets are formed and extruded from the muscle cytoplasm into the hemolymph; this process may account for some of the decrease in muscle fiber mass and may represent a developmental mechanism for recycling nutrients. As the fibers shrink, the thick basal lamina is thrown into folds. Phagocytic hemocytes (granulocytes) congregate in clusters over the surface of the degenerating fibers and appear to remove specifically the basal lamina. The timely removal of the thick larval basal lamina may be essential for subsequent fusion of myoblasts to the residual larval myofibers. The contractile elements within the degenerating muscle fibers become disorganized but are not dysfunctional at the end of the first 12 h after the pupal ecdysis. Tracheoles withdraw from intimate contact with each muscle fiber in its clefts and T-tubules and associate in groups adjacent to it. Mitochondria appear to be degenerating. These structural changes are concurrent with a previously observed decline in resting potential and suggest that a significant change in the electrical properties of the muscle fibers should be expected as well.

Quantal Secretion and Nerve-Terminal Cable Properties at Neuromuscular Junctions in an Amphibian (Bufo marinus)

1999 ◽  
Vol 81 (3) ◽  
pp. 1135-1146 ◽  
Author(s):  
G. T. Macleod ◽  
L. Farnell ◽  
W. G. Gibson ◽  
M. R. Bennett
Keyword(s):  
Nerve Terminal ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Current Injection ◽  
Bufo Marinus ◽  
Motor Nerve Terminal ◽  
Terminal Branch ◽  
Quantal Release ◽  
Cable Properties ◽  
Test Electrode

Quantal secretion and nerve-terminal cable properties at neuromuscular junctions in an amphibian ( Bufo marinus). The effect of a conditioning depolarizing current pulse (80–200 μs) on quantal secretion evoked by a similar test pulse at another site was examined in visualized motor-nerve terminal branches of amphibian endplates ( Bufo marinus). Tetrodotoxin (200 nM) and cadmium (50 μM) were used to block voltage-dependent sodium and calcium conductances. Quantal release at the test electrode was depressed at different distances (28–135 μm) from the conditioning electrode when the conditioning and test pulses were delivered simultaneously. This depression decreased when the interval between conditioning and test current pulses was increased, until, at an interval of ∼0.25 ms, it was negligible. At no time during several thousand test-conditioning pairs, for electrodes at different distances apart (28–135 μm) on the same or contiguous terminal branches, did the electrotonic effects of quantal release at one electrode produce quantal release at the other. Analytic and numerical solutions were obtained for the distribution of transmembrane potential at different sites along terminal branches of different lengths for current injection at a point on a terminal branch wrapped in Schwann cell, in the absence of active membrane conductances. Solutions were also obtained for the combined effects of two sites of current injection separated by different time delays. This cable model shows that depolarizing current injections of a few hundred microseconds duration produce hyperpolarizations at ∼30 μm beyond the site of current injection, with these becoming larger and occurring at shorter distances the shorter the terminal branch. Thus the effect of a conditioning depolarizing pulse at one site on a subsequent test pulse at another more than ∼30 μm away is to substantially decrease the absolute depolarization produced by the latter, provided the interval between the pulses is less than a few hundred microseconds. It is concluded that the passive cable properties of motor nerve terminal branches are sufficient to explain the effects on quantal secretion by a test electrode depolarization of current injections from a spatially removed conditioning electrode.

scholarly journals Acetylcholinesterase from the motor nerve terminal accumulates on the synaptic basal lamina of the myofiber.

1991 ◽  
Vol 115 (3) ◽  
pp. 755-764 ◽  
Author(s):  
L Anglister
Keyword(s):  
Basal Lamina ◽  
Ache Activity ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Synaptic Cleft ◽  
Motor Nerve Terminal ◽  
Nerve Terminals ◽  
Axon Terminals ◽  
Muscle Nerve ◽  
Almost All

Acetylcholinesterase (AChE) in skeletal muscle is concentrated at neuromuscular junctions, where it is found in the synaptic cleft between muscle and nerve, associated with the synaptic portion of the myofiber basal lamina. This raises the question of whether the synaptic enzyme is produced by muscle, nerve, or both. Studies on denervated and regenerating muscles have shown that myofibers can produce synaptic AChE, and that the motor nerve may play an indirect role, inducing myofibers to produce synaptic AChE. The aim of this study was to determine whether some of the AChE which is known to be made and transported by the motor nerve contributes directly to AChE in the synaptic cleft. Frog muscles were surgically damaged in a way that caused degeneration and permanent removal of all myofibers from their basal lamina sheaths. Concomitantly, AChE activity was irreversibly blocked. Motor axons remained intact, and their terminals persisted at almost all the synaptic sites on the basal lamina in the absence of myofibers. 1 mo after the operation, the innervated sheaths were stained for AChE activity. Despite the absence of myofibers, new AChE appeared in an arborized pattern, characteristic of neuromuscular junctions, and its reaction product was concentrated adjacent to the nerve terminals, obscuring synaptic basal lamina. AChE activity did not appear in the absence of nerve terminals. We concluded therefore, that the newly formed AChE at the synaptic sites had been produced by the persisting axon terminals, indicating that the motor nerve is capable of producing some of the synaptic AChE at neuromuscular junctions. The newly formed AChE remained adherent to basal lamina sheaths after degeneration of the terminals, and was solubilized by collagenase, indicating that the AChE provided by nerve had become incorporated into the basal lamina as at normal neuromuscular junctions.

Comparison of slow larval and fast adult muscle innervated by the same motor neurone

1980 ◽  
Vol 84 (1) ◽  
pp. 103-118
Author(s):  
M. B. Rheuben ◽  
A. E. Kammer
Keyword(s):  
Developmental Stages ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Thick Filament ◽  
Motor Neurone ◽  
Muscle Fibre Types ◽  
Thin Filaments ◽  
Adult Muscle ◽  
Motor Neurones ◽  
Two Stages

1. Muscles innervated by an identified set of motor neurones were compared between larval and adult stages. 2. The structure of the larval muscle is typically tonic: long sarcomeres, irregular Z-bands, and 10-12 thin filaments around each thick filament. The structure of the adult muscle is phasic: 3-4 micrometers sarcomeres, regular Z-bands, 6-8 thin filaments around each thick filament, and large mitochondrial volume. 3. The tensions produced by these muscles were correspondingly different. The larval twitch was about 7 times slower and the tetanus/twitch ratio 10 times greater than those of the adult. 4. No structural or physiological differences were observed in the neuromuscular junctions of the two stages. 5. The relatively unchanging functional relationship of a single motor neurone with two different muscle fibre types during two developmental stages is compared with the converse situation in which it has been reported that implantation of a different type of motor nerve into a muscle modifies contractile properties.

scholarly journals Effects of Vocal Training on Thyroarytenoid Muscle Neuromuscular Junctions and Myofibers in Young and Older Rats

2020 ◽  
Author(s):  
Adrianna C Shembel ◽  
Charles Lenell ◽  
Sophia Chen ◽  
Aaron M Johnson
Keyword(s):  
Neuromuscular Junction ◽  
Muscle Fiber ◽  
Acoustic Analysis ◽  
Neuromuscular Junctions ◽  
Fiber Type ◽  
Male Rats ◽  
Brown Norway ◽  
Control Group ◽  
Vocal Training ◽  
Thyroarytenoid Muscle

Abstract The purpose of this investigation was to determine the effects of vocal training on neuromuscular junction (NMJ) morphology and muscle fiber size and composition in the thyroarytenoid muscle, the primary muscle in the vocal fold, in younger (9-month) and older (24-month) Fischer 344 × Brown Norway male rats. Over 4 or 8 weeks of vocal training, rats of both ages progressively increased their daily number of ultrasonic vocalizations (USVs) through operant conditioning and were then compared to an untrained control group. Neuromuscular junction morphology and myofiber size and composition were measured from the thyroarytenoid muscle. Acoustic analysis of USVs before and after training quantified the functional effect of training. Both 4- and 8-week training resulted in less NMJ motor endplate dispersion in the lateral portion of the thyroarytenoid muscle in rats of both ages. Vocal training and age had no significant effects on laryngeal myofiber size or type. Vocal training resulted in a greater number of USVs with longer duration and increased intensity. This study demonstrated that vocal training induces laryngeal NMJ morphology and acoustic changes. The lack of significant effects of vocal training on muscle fiber type and size suggests vocal training significantly improves neuromuscular efficiency but does not significantly influence muscle strength changes.

Structural and functional changes of frog neuromuscular junctions in high calcium solutions

1971 ◽  
Vol 178 (1053) ◽  
pp. 407-415 ◽  
Keyword(s):  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Neuromuscular Junctions ◽  
Motor Nerve ◽  
Secretory Response ◽  
Spontaneous Release ◽  
Functional Changes ◽  
High Calcium ◽  
Release Of Acetylcholine ◽  
Evoked Transmitter Release

When frog muscles are exposed for several hours to a solution of isotonic calcium chloride, the secretory response of the motor nerve terminals to imposed depolarization ultimately fails and the rate of spontaneous release of acetylcholine also declines towards zero. The failure of depolarization-evoked transmitter release is irreversible while spontaneous release reappears, though in highly abnormal fashion, when the muscle is returned to a normal ionic medium. Examination of motor end-plates, during various stages of calcium treatment, shows that there is gradual intra-axonal agglutination of synaptic vesicles which is only very incompletely reversible. This effect is presumably the consequence of gradual entry and intracellular accumulation of calcium ions. Analogous treatment with isotonic magnesium, while resulting in immediate loss of evoked transmitter release, does not lead to progressive agglutination of synaptic vesicles, nor to irreversible impairment of the secretory response of the nerve terminal. The possible relations between structural and functional changes during calcium and magnesium treatment are discussed.

Cellular electrophysiological marker of irreversible ischemic myocardial injury

1978 ◽  
Vol 235 (5) ◽  
pp. H559-H568
Author(s):  
J. McGee ◽  
D. H. Singer ◽  
R. E. Eick ◽  
R. Kloner ◽  
N. Belic ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Resting Potential ◽  
Morphological Evidence ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Coronary Ligation ◽  
Microscopic Studies ◽  
Anesthetized Dogs ◽  
Definition Of ◽  
Irreversible Injury

Glass microelectrode studies on posterior papillary muscle (PPM) slice preparations from 20 pentobarbital-anesthetized dogs (15 subjected to prior circumflex coronary artery ligation, 5 to sham ligation) have resulted in the definition of an electrophysiological marker of irreversible ischemic injury, namely, findings of areas composed of cells unable to generate a significant resting potential (less than -25) mV), designated "electrically inactive areas." Electrically inactive areas were essentially confined to PPM from dogs with circumflex coronary ligation; the incidence and distribution of the areas was related to duration of ischemia. Correlative phase- and light-microscopic studies demonstrated close correspondence between such areas and morphological evidence of irreversible ischemic injury. Analysis of frequency and distribution of electrically inactive areas permits quantitative assessment of the extent and spatial distribution of irreversible injury. This method has been used to quantitate injury in PPM from dogs that had been subjected to ligation for varying time periods. The potential utility of this method for evaluation of interventions designed to protect against ischemic injury and to assess electrical properties of surviving cells is considered.

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