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PubMed1993

Interactions between nerve and muscle: synapse elimination at the developing neuromuscular junction.

Studies of synaptogenesis at the developing neuromuscular junction have provided a wealth of information regarding the various mechanisms that are involved in the formation of synaptic connections. In addition to synapse formation, however, the mature pattern of innervation at the neuromuscular junction (and elsewhere in the nervous system) depends on a significant loss of synaptic connections during development. The molecular mechanisms involved in the process of synapse elimination are not understood. Recent work at the neuromuscular junction suggests that changes in the postsynaptic cell may be necessary in order for nerve terminals to be eliminated. Thus, in contrast to synapse formation in which an axon terminal initiates a cascade of changes leading to the formation of pre- and postsynaptic specializations, synapse elimination may be initiated by local changes in the postsynaptic cell that disassemble the postsynaptic apparatus and ultimately remove the overlying terminal. In this review, we wish to examine the potential role that some of the factors involved in synapse formation might play in the less-well-understood phenomenon of synapse elimination.

Aging↗
PubMed2003

Localizing synaptic mRNAs at the neuromuscular junction: it takes more than transcription.

The neuromuscular junction has been used for several decades as an excellent model system to examine the cellular and molecular events involved in the formation and maintenance of a differentiated chemical synapse. In this context, several laboratories have focused their efforts over the last 15 years on the important contribution of transcriptional mechanisms to the regulation of the development and plasticity of the postsynaptic apparatus in muscle fibers. Converging lines of evidence now indicate that post-transcriptional events, operating at the level of mRNA stability and targeting, are likely to also play key roles at the neuromuscular junction. Here, we present the recent findings highlighting the role of these additional molecular events and extend our review to include data showing that post-transcriptional events are also important in the control of the expression of genes encoding synaptic proteins in muscle cells placed under different conditions. Finally, we discuss the possibility that mis-regulation of post-transcriptional events can occur in certain neuromuscular diseases and cause abnormalities of the neuromuscular junction.

Animals↗
PubMed1976

An electron microscopic study of the neuromuscular junction in the myotomes of larval lamprey, Lampetra japonica.

The neuromuscular junction in the myotomes of larval and adult lampreys, Lampetra japonica, was studied with the electron microscope. In larval lampreys of 26 days after artificial insemination, the myotome consists of triangular lamellae of muscle cell with their bases laterally and apexes medially oriented and placed one on the other. The lateral aspect of the myotome is covered by a layer of flattened cell, and the other aspect is covered by an external lamina which does not extend into the intercellular space between adjacent cells within a myotome. A bundle of thin axons was found in a depression at the middle of medial edge (apex) of each muscle lamella of the myotome and neuromuscular junction was formed here. No nerve endings were found at the myoseptal ends or at the lateral borders of the muscle lamellae. Enlarged axon terminals contained numerous clear vesicles with a few cored vesicles, mitochondria and neurofilaments. The presynaptic axolemma was separated from the postsynaptic sarcolemma by an interspace (50-55 mmu wide) with an interposed external lamina. In the trunk musculature of adult lampreys, nerve endings were found on the surface of the parietal fibers whereas they were seen on both the myoseptal ends near the myotendinous junction along the medial border of each central fiber. Thickening and enhancement in the electron density and accumulation of filamentous material on the sarcoplasmic surface of the postsynaptic sarcolemma were noted in both the larval and adult lampreys. Any other specific alterations were not found on both the pre- and postsynaptic membrane in the neuromuscular junctions of larval and adult lampreys. A brief comment was made on the relationship in development of the characteristic muscle units and patterns of the motor innervation in the larval and adult lampreys. The significance of the neuromuscular junction in the very young larvae reported here was also discussed in respect to the evolution of the neuromuscular junction, particularly in lower chordates, and it was presumed to be the most primitive pattern of innervation in the vertebrate skeletal muscle.

Animals↗
PubMed1994

Time course of miniature currents in regenerating neuromuscular junctions of the cockroach Periplaneta americana.

Miniature excitatory junctional currents in regenerating neuromuscular junctions have been recorded from the denervated leg muscle fibers of the cockroach, Periplaneta americana with an external focal electrode. Miniature currents first reappeared after 21 days after denervation at 26 degrees C. These currents occurred at a lower frequency and had a slower time course than miniature currents at normal junctions. The decay time constant of the falling phase of the earliest current was more than twice the control and the mean amplitude was less than half of the control. The decay time constant of the currents became shorter and their amplitude increased with increasing time after regeneration and approached control values at about 60 days after crushing the nerve. During regeneration of neuromuscular junctions, the falling phase of the miniature currents was always along a single exponential just as in the control. The observed change in the decay time constant of the currents suggests that the open time of the overall population of synaptic receptor-channels increases after denervation and returns to the control with time.

Animals↗
PubMed1991

Plasticity of presynaptic and postsynaptic elements of neuromuscular junctions repeatedly observed in living adult mice.

In order to assay the extent of ongoing synaptic remodelling in adult mouse neuromuscular junctions, dynamic structural changes of identified neuromuscular junctions were monitored in vivo over periods up to three months. Nerve terminal outgrowths as small as 1 micron were detectable with a new fluorescent tetanus toxin C-fragment stain combined with fluoresceinated alpha-bungarotoxin to stain postsynaptic acetylcholine receptors. With limited illumination, the new stain did not affect miniature endplate potential frequency, nor morphometric parameters of repeatedly observed neuromuscular junctions. At each observation, areas of presynaptic nerve terminal extending beyond underlying acetylcholine receptor ('preprojections'), and areas of acetylcholine receptor without overlying nerve terminal ('postprojections') were measured. Regions of the neuromuscular junction in which nerve terminal-postsynaptic acetylcholine receptor complexes either 'lengthened' or 'shortened' between observations were also measured. The total area of pre- and postprojections (relative to total junctional area) remained the same over three months but most had been replaced; only 20% of preprojections gave rise to lengthenings, the rest retracted or were unchanged. Lengthening and shortening of branches were about 1-2% of junctional area per month. These more permanent changes occurred against a background of ongoing transient nerve terminal outgrowth and retraction (which constituted 80% of all neuromuscular junction shape changes from one observation to the next, compared with 20% for the postsynaptic component). Breaks in the continuity of the underlying acetylcholine receptor were also observed between observations as were instances where acetylcholine receptor continuity was re-established. A newly observed form of plasticity was a shift in position and angle of pre-existing branches. Establishment of new acetylcholine receptor-positive synaptic regions was mostly preceded by nerve terminal outgrowth on the previous observation. In animals in which spontaneous wheel-running increased locomotor activity approximately tenfold over a period of 35 days, the findings were identical to those in unexercised mice. In summary, in the adult neuromuscular junction, the nerve terminal, not the postsynaptic component, is the dynamic entity, continually changing shape on the scale of micrometers, with relatively small permanent changes. These ongoing exploratory excursions may supply the substrate for synaptic plasticity, which would involve regulation of the dynamics or stability of nerve outgrowth.

Animals↗
PubMed1989

Silver cholinesterase immunocytochemistry: a new neuromuscular junction stain.

Evaluation of morphological alterations at the neuromuscular junction associated with sprouting or other pathological changes has been limited by the inability to visualize simultaneously the multiple cell types that make up a junction. A new combined stain for the concurrent demonstration of motor nerve terminals, cholinesterase, and Schwann cell myelin and other antigens at neuromuscular junctions using bromoindoxyl acetate dye staining for cholinesterase, silver-gold impregnation for nerve terminals, and immunocytochemistry of selected antigens is described. The clarity of the stain permits graphic demonstration of the alteration of neuromuscular junction components during sprouting as well as other pathological changes.

Animals↗
PubMed1996

Alterations in neuromuscular junction morphology during fast-to-slow transformation of rabbit skeletal muscles.

Chronic low frequency stimulation of motor nerves results in transformation of muscle fibre phenotype from fast- to slow-twitch. We examined the light and electron microscopic structure of neuromuscular junctions in normally fast twitch muscles, tibialis anterior and extensor digitorum longus of rabbit after 3 weeks of stimulation to determine whether synaptic structure is also modified during fibre type transformation. Neuromuscular junctions of stimulated and unstimulated (control) tibialis anterior and extensor digitorum longus muscles and unstimulated slow twitch soleus muscle were visualized with rhodamine-conjugated alpha-bungarotoxin. Video light microscopic images of neuromuscular junctions were digitized to allow quantification of their surface areas, perimeters, lengths and widths. Three weeks of stimulation resulted in a decrease in the maximal velocity of muscle fibre shortening and augmentation of mitochondrial volume in fast muscles, demonstrating the efficacy of the stimulation protocol employed in altering muscle fibre phenotype. Neuromuscular junctions of control tibialis anterior and extensor digitorum longus are thin, compact, and continuous, with complex branching patterns. In contrast, those of slow-twitch soleus are thicker and discontinuous. Neuromuscular junctions in control tibialis anterior and extensor digitorum longus are larger than those in soleus. Three weeks of stimulation causes a marked decrease in the size of neuromuscular junctions in tibialis anterior and extensor digitorum longus, as reflected in the significant reduction in neuromuscular junction surface area, length and width. Electron microscopy of these junctions suggests that secondary postsynaptic folds in stimulated muscles are more closely spaced. Also, axon terminals of stimulated muscles appear to contain more densely packed synaptic vesicles and mitochondria than controls. Decreases in neuromuscular junction dimensions can be partly explained by muscle fibre atrophy. However, the decrease in neuromuscular junction size is proportionately greater than that of muscle fibre diameter in both muscles, indicating that factors other than fibre atrophy may contribute to the reduced neuromuscular junction size in stimulated muscles. Neuromuscular junctions of stimulated tibialis anterior and extensor digitorum longus muscles exhibit some features characteristic of normal soleus neuromuscular junctions, indicating structural adaptations consistent with the altered muscle fibre phenotype. On the other hand, neuromuscular junctions of 3 week stimulated tibialis anterior and extensor digitorum longus and their synaptic branches remain as thin and continuous as those of unstimulated controls, suggesting that the transformation of neuromuscular junctions towards a morphology characteristic of slow muscle, is only partial. These results demonstrate that an altered pattern of impulse activity cause significant synaptic remodelling in adult rabbit skeletal muscles.

Animals↗
PubMed1987

Incorporation of vesicular antigens into the presynaptic membrane during exocytosis at the frog neuromuscular junction: a light and electron microscopy immunochemical study.

We have studied the incorporation of vesicular membrane antigens into the presynaptic membrane during exocytosis of neurotransmitter at the frog neuromuscular junction. In a preliminary series of experiments, we first confirmed by electron microscopy that the synaptic vesicles are labelled following incubation with rabbit antisynaptic vesicle antibody of neuromuscular junction cross sections (cytoplasm and organelles reached by the antibodies). In a second series of experiments, intact neuromuscular junctions were stimulated with black widow spider venom and fixed with paraformaldehyde. The presence or absence of vesicular antigens in the presynaptic membrane was monitored with rabbit antisynaptic vesicle antibody and revealed with a second antibody coupled to peroxidase. In light microscopy, the labelled neuromuscular junctions are almost completely restricted to muscles stimulated with black widow spider venom and incubated with rabbit antisynaptic vesicle antibody. Only a few control muscles (not stimulated with black widow spider venom, but incubated with rabbit antisynaptic vesicle antibody) had labelled neuromuscular junctions. All control neuromuscular junctions, not incubated with rabbit antisynaptic vesicle antibody were unlabelled. Electron microscopy indicated that it is the presynaptic membrane of intact stimulated neuromuscular junctions which is labelled. In these intact neuromuscular junctions, the synaptic vesicles are usually unlabelled. Electron microscopy also indicated that the presynaptic membrane of only one type of control junctions (not stimulated with black widow spider venom, but incubated with rabbit antisynaptic vesicle antibody) is rarely and weakly labelled. Other types of controls (not incubated with rabbit antisynaptic vesicle antibody) are never labelled. Therefore our results are consistent with the incorporation of vesicular antigens into the plasma membrane during exocytosis produced by the black widow spider venom. The low level of labelling of unstimulated neuromuscular junctions suggest a rather complete retrieval of the vesicular proteins during endocytosis.

Animals↗
PubMed2002

Calcium channel subtypes contributing to acetylcholine release from normal, 4-aminopyridine-treated and myasthenic syndrome auto-antibodies-affected neuromuscular junctions.

1 Acetylcholine release at the neuromuscular junction relies on rapid, local and transient calcium increase at presynaptic active zones, triggered by the ion influx through voltage-dependent calcium channels (VDCCs) clustered on the presynaptic membrane. Pharmacological investigation of the role of different VDCC subtypes (L-, N-, P/Q- and R-type) in spontaneous and evoked acetylcholine (ACh) release was carried out in adult mouse neuromuscular junctions (NMJs) under normal and pathological conditions. 2 omega-Agatoxin IVA (500 nM), a specific P/Q-type VDCC blocker, abolished end plate potentials (EPPs) in normal NMJs. However, when neurotransmitter release was potentiated by the presence of the K(+) channel blocker 4-aminopyridine (4-AP), an omega-agatoxin IVA- and omega-conotoxin MVIIC-resistant component was detected. This resistant component was only partially sensitive to 1 micro M omega-conotoxin GVIA (N-type VDCC blocker), but insensitive to any other known VDCC blockers. Spontaneous release was dependent only on P/Q-type VDCC in normal NMJs. However, in the presence of 4-AP, it relied on L-type VDCCs too. 3 ACh release from normal NMJs was compared with that of NMJs of mice passively injected with IgGs obtained from patients with Lambert-Eaton myasthenic syndrome (LEMS), a disorder characterized by a compromised neurotransmitter release. Differently from normal NMJs, in LEMS IgGs-treated NMJs an omega-agatoxin IVA-resistant EPP component was detected, which was only partially blocked by calciseptine (1 micro M), a specific L-type VDCC blocker. 4 Altogether, these data demonstrate that multiple VDCC subtypes are present at the mouse NMJ and that a resistant component can be identified under 'pharmacological' and/or 'pathological' conditions.

4-Aminopyridine↗
PubMed1974

Studies of excitable membranes. I. Macromolecular specializations of the neuromuscular junction and the nonjunctional sarcolemma.

The neuromuscular junctions and nonjunctional sarcolemmas of mammalian skeletal muscle fibers were studied by conventional thin-section electron microscopy and freeze-fracture techniques. A modified acetylcholinesterase staining procedure that is compatible with light microscopy, conventional thin-section electron microscopy, and freeze-fracture techniques is described. Freeze-fracture replicas were utilized to visualize the internal macromolecular architecture of the nerve terminal membrane, the chemically excitable neuromuscular junction postsynaptic folds, and the electrically excitable nonjunctional sarcolemma. The nerve terminal membrane is characterized by two parallel rows of 100-110-A particles which may be associated with synpatic vesicle fusion and release. On the postsynpatic folds, irregular rows of densely packed 110-140-A particles were observed and evidence is assembled which indicates that these large transmembrane macromolecules may represent the morphological correlate for functional acetylcholine receptor activity in mammalian motor endplates. Differences in the size and distribution of particles in mammalian as compared with amphibian and fish postsynaptic junctional membranes are correlated with current biochemical and electron micrograph autoradiographic data. Orthogonal arrays of 60-A particles were observed in the split postsynaptic sarcolemmas of many diaphragm myofibers. On the basis of differences in the number and distribution of these "square" arrays within the sarcolemmas, two classes of fibers were identified in the diaphragm. Subsequent confirmation of the fiber types as fast- and slow-twitch fibers (Ellisman et al. 1974. J. Cell Biol.63[2, Pt. 2]:93 a. [Abstr.]) may indicate a possible role for the square arrays in the electrogenic mechanism. Experiments in progress involving specific labeling techniques are expected to permit positive identification of many of these intriguing transmembrane macromolecules.

Acetylcholine↗
PubMed1989

[An ultrastructural study of the neuromuscular junctions of the cat intrinsic laryngeal muscles. I. Denervation and reinnervation].

Morphological changes of the neuromuscular junctions induced by denervation and reinnervation have been investigated electronmicroscopically using cat intrinsic laryngeal muscles. Two experiments were performed: 1. simple transection of the unilateral recurrent laryngeal nerve at the level of the second tracheal ring; 2. neurorrhaphy immediately after the transection at the same level. 1. All the ipsilateral intrinsic laryngeal muscles except for the cricothyroid muscle were denervated 48 hours after the transection of the recurrent laryngeal nerve. In the denervated neuromuscular junctions some primary synaptic clefts were narrowed and others were flattened, while the secondary synaptic clefts were structurally preserved. 2. Some of the regenerating axons returned to the neuromuscular junctions 3 weeks after neurorrhaphy, and all the muscle fibres were reinnervated after 6 weeks. The structural features of the reinnervated neuromuscular junctions were as follows; 1) synaptic vesicles of the nerve terminals were more densely observed, 2) the original postsynaptic membranes were only partially in contact with the regenerated nerve terminals. These conditions persisted until 22 weeks after neurorrhaphy, when the appearance of remyelination was found in the vicinity of the neuromuscular junctions. Using an evoked electromyogram, the presence of neuromuscular transmission was observed 3 weeks after neurorrhaphy, indicating that the structural maturation of the neuromuscular junction was not necessary for neuromuscular transmission.

Animals↗
PubMed1985

Quantitative comparison of the structural features of slow and fast neuromuscular junctions in Manduca.

The multiterminal slow and fast neuromuscular junctions of the moth Manduca sexta were compared using scanning, thin-section, and freeze-fracture techniques to see what structural features might underlie their functional differences. Slow neuromuscular junctions, here formed on tonic muscle fibers, produce a facilitating e.j.p. the amplitude of which is 1/5 to 1/3 the size of a fast excitatory junction potential (EJP) and the duration of which is nearly four times longer. A slow junction consists of a single terminal branch that is shorter in length than either of the pair of branches that a fast junction forms close together on the muscle fiber. Within the junction, slow nerve terminals exhibit longer, more frequent constrictions and are very varicose compared with fast. Since fast larval junctions on tonic muscle fibers are also varicose (Schaner and Rheuben, 1985), this is unlikely to represent an intrinsic property of the nerve. However, calculations of the length constants of the varicose versus nonvaricose shapes indicate that the effect of passive cable properties on normal functioning may act to limit the length of the slow terminals more than that of fast. Even though the varicose shape can be predicted to prolong the time course of the EJP, calculations show that, at the measured length, this would not explain the very long EJP that is observed. Within the neuromuscular junctions, the synapses are characterized on the muscle membrane by a patch of densely packed particles on the external leaflet and on the nerve membrane by a single linear active zone. The total number of synapses per slow junction is about 1/3 that of fast junctions. There is a weak correlation between average area of the individual postsynaptic particle patches and cross-sectional area of the muscle fibers that transcends nerve and muscle fiber types. The average lengths of active zones from the two types do not differ significantly. However, the number of particles per active zone in slow junctions is about 55% of the number in fast active zones. Chemically fixed slow nerve terminals have a greater density of synaptic vesicles remaining than do fast. If a proportion of the active zone particles represent structures directly involved in the probability of transmitter release, such as Ca++ channels, then the latter two characteristics may jointly reflect differences in capability to release and mobilize transmitter that would partly explain the different EJP amplitude and facilitation properties.

Lepidoptera↗
PubMed1992

Localization of dystrophin and dystrophin-related protein at the electromotor synapse and neuromuscular junction in Torpedo marmorata.

The immunological identification of dystrophin isoforms at the neuromuscular junction and Torpedo marmorata electromotor synapse was attempted using various antibodies. A polyclonal antibody raised against electrophoretically purified dystrophin from T. marmorata electrocyte has been thoroughly investigated. This antibody recognized dystrophin in the electric tissue as well as sarcolemmal and synaptic neuromuscular junction dystrophin in all studies species (T. marmorata, rat, mice and human) at serum dilutions as high as 1:10,000. At variance, no staining of either the sarcolemma or neuromuscular junction was observed in Duchenne muscular dystrophy or mdx mice skeletal muscles. In these muscles, other members of the dystrophin superfamily, in particular the dystrophin-related protein(s) encoded by autosomal genes are present. These data thus demonstrate the specificity of our antibodies for dystrophin. Anti-dystrophin-related protein antibodies [Khurana et al. (1991) Neuromusc. Disorders 1, 185-194] which gave a strong immunostaining of the neuromuscular junction in various species, including T. marmorata, cross-reacted weakly with the postsynaptic membrane of the electrocyte. Taken together, these observations are in favor of the existence of a protein very homologous to dystrophin at the electromotor synapse in T. marmorata, whereas both dystrophin and dystrophin-related protein co-localize at the neuromuscular junction as in all species studied. The electrocyte thus offers the unique opportunity to study the interaction of dystrophin with components of the postsynaptic membrane.

Animals↗
PubMed2006

[Pathological changes in neuromuscular junction during ischemia-reperfusion in rat skeletal muscle].

OBJECTIVE: To investigate the pathological changes in the neuromuscular junction during ischemia-reperfusion (IR) in the skeletal muscle. METHODS: Forty-eight healthy adult Wistar rats (24 male, 24 female) were equally randomised into the following 6 groups: Group A (control group): no ischemia-reperfusion; Group B: ischemia by clamping the blood vessels of the right hindlimb for 3 hours; Group C: ischemia by clamping for 4.5 hours; Group D: ischemia by the clamping for 4.5 hours followed by reperfusion for 1.5 hours; Group E: ischemia for 4.5 hours followed by reperfusion for 24 hours; and Group F: ischemia for 4. 5 hours followed by reperfusion for 2 weeks. Then, the medial head of the gastrocnemius muscle flap model was applied to the right hindlimb of each rat. The medial head of the gastrocnemius muscle was isolated completely,leaving only the major vascular pedicle, nerve and tendons intact. The proximal and distal ends (tendons) were ligated while the vessel pedicle was clamped. And then, Parameters of the muscle (performance, contraction index, colour, edema, bleeding) were observed. The muscle harvested was stained with gold chloride (AuCl3) and the enzyme histochemistry assay (succinate dehydrogenase combined with acetylcholine esterase) was performed. Morphology and configuration of the neuromuscular junction were observed during the ischemia-reperfusion injury by means of the AuCl3 staining. The result of the enzymehistochemical reactions was quantitatively analyzed with the computer image-analysis system. And then, additional 5 rats were prepared for 3 different models identical with those in Groups A, C and E separately. The specimens were harvested from each rat and were stained with HE and AuCl3, and they were examined under the light microscope. RESULTS: During the period of ischemia, the skeletal muscle of Group B showed the colour of purple and edema. The colour and edema became worse in Group C,while dysfunction of elasticity and contraction appeared obviously with plenty of dark red hemorrhagic effusion at the same time. After reperfusion,the color and edema of muscle in Group D became improved while the elasticity and function of contraction was not improved. Hemorrhagic effusion of Group D turned clearer and less than Group C. Group E was similar to Group D in these aspects of muscle except for much less hemorrhagic effusion. Skeletal muscle in Group F showed colour of red alternating with white, adhesion, contracture of muscle, exposure of necrotic yellow tissue and almost lost all its functions. The AuCl3 staining showed that during IR, necrosis of the myocytes was followed by degeneration of their neuromuscular junctions, and finally the nerve fibers attached to these neuromuscular junctions were disrupted like the withering of leaves. The enzyme histochemistry assay showed that there was no significant difference in the level of acetylcholine esterase between the ischemic group (Groups B and C) and the control group (Group A) (P>0.05). However, the level of acetylcholine esterase in all the reperfused groups (Groups D, E and F) decreased significantly when compared with the control group (Group A) and the ischemic groups (Groups B and C) (P<0.01). CONCLUSION: The distribution of the nerve fibers and the neuromuscular junctions in the mass of the muscles is almost like the shape of a tree. The neuromuscular junction seems to be more tolerant for ischemia than the myocyte. Survival of the neuromuscular junction depends on its myocytes alive. Therefore, an ischemia-reperfusion injury will not be controlled unless an extensive debridement of the necrotic muscle is performed.

Animals↗
PubMed1983

Distribution and turnover rate of acetylcholine receptors throughout the junction folds at a vertebrate neuromuscular junction.

The distribution and turnover rate of acetylcholine receptors labeled with 125I-alpha-bungarotoxin were examined in innervated mouse sternomastoid muscle by electron microscope autoradiography using the "mask" analysis procedure. We compared the total population of receptors with receptors newly inserted at the junction 2 d after inactivation with nonradioactive alpha-bungarotoxin, both at the top (thickened) region of the postjunctional folds (pjm) and the nonthickened bottom folds. We found that the receptor site density was approximately 10 times greater on the thickened pjm than on the nonthickened bottom folds for both total and newly inserted receptors. This ratio does not change significantly during a 6-d period after labeling the new receptors. Furthermore, calculated values for turnover time of receptors show that both total and newly inserted receptors at both regions of the junctional folds have half-lives for degradation within the range given in the literature for slow junctional receptors. These data exclude a simple migration model whereby receptors are preferentially inserted in the nonthickened region of the junctional folds and then migrate into the thickened membrane at a rate equal to the turnover rate of the receptors.

Animals↗
PubMed2000

Morphological characteristics of neuromuscular junctions of the opossum (Didelphis albiventris) extraocular muscles: a scanning-electron-microscopic study.

Three types of neuromuscular junctions were described in the extraocular muscles of the opossum. The present study demonstrates the three-dimensional characteristics of these neuromuscular junctions after HCl connective tissue digestion. Adult opossum of both sexes were used and the neuromuscular junctions of the extraocular muscles were examined after removal of the intramuscular connective tissue and basal layer. This material was examined with a scanning electron microscope. Two types of 'en plaque' neuromuscular junction were described: the continuous type revealed elongated and branched primary synaptic grooves separated from each other by sarcolemma protuberances with different sizes, and the discontinuous or punctiform type which presents very shallow and discontinuous grooves when compared with the former. The multiple neuromuscular junctions were observed as two or three junctions associated with the same muscular fiber. The multiple junctions were present in thin fibers (around 11 microm caliber); the en plaque junctions were associated with large diameter fibers (around 21 microm). This study confirms and reveals the detailed morphological characteristics of the three neuromuscular junction types previously described by transmission electron microscope in the extraocular muscles of opossum.

Animals↗
PubMed1978

The role of muscle activity in the differentiation of neuromuscular junctions in slow and fast chick muscles.

The differentiation of neuromuscular junctions of multiply innervated, slow anterior latissimus dorsi (ALD) and focally innervated, fast, posterior latissimus dorsi (PLD) muscles was studied in normal and curarized chick embryos. At 16 days of incubation, fibres of both muscles are contacted by several axon profiles, the number of which falls with age. In 18-day-old embryos individual endplates in ALD are usually contacted by three axon profiles, whereas in PLD, endplates are contacted only by a single large terminal profile. At this time, there is already a significant accumulation of cell organelles in the postsynaptic area. Treatment of embryos with curare during the 7th and 12th day of incubation delays the differentiation of the neuromuscular junction in both muscles. The paralysis dramatically affects the decrease of the number of axon profiles at individual endplates in both muscles. At 16 days the number of axon profiles was greater in embryos treated with curare than in the untreated controls. At 18 days when the number of axon profiles normally decreases, the endplates of both types of curarized muscles have an even greater number of axon profiles than at 16 days. Endplates in curarized PLD had up to 13 and in curarized ALD up to 12 axon profiles. The effects of curare gradually wore off and when the movements of the embryos again became more vigorous, the normal differentiation of neuromuscular junctions continued. At 21 days of incubation many embryos recover from curare and show endplates of normal appearance in both muscles. These results suggest that activity of the muscle is essential for the maturation of the neuromuscular junctions.

Animals↗