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At least 19 recordsLinked to original sources
PubMed1978

Synaptic vesicles and microtubules in frog motor endplates.

Motor endplates of the cutaneous pectoris skeletal muscle of the frog have been examined by electron microscopy using a new technique. This involves pretreatment with an albumin solution, followed by fixation with 4% unbuffered tetroxide. A small proportion of the endplate axonal ramifications show microtubules clothed in synaptic vesicles and focused on the presynaptic membrane, in particular on the active zones. The microtubules run in the presynaptic cytoplasm either parallel to or across the active zones. These two sets of microtubules cross each other at the active zones, which lie opposite the dips in the post-junctional folds. The possibility that the microtubules are involved in the translocation of synaptic vesicles to the active zone is discussed.

Albumins↗
PubMed1997

Human facial muscles: dimensions, motor endplate distribution, and presence of muscle fibers with multiple motor endplates.

BACKGROUND: Extrafusal muscle fibers of human striated skeletal muscles are known to have a uniform innervation pattern. Motor endplates (MEP) of the "en plaque" type are located near the center of muscle fibers and distributed within the muscles in a narrow band. The aim of this study was to evaluate the innervation pattern of human facial muscles and compare it with that of skeletal muscles. METHODS: Ten facial muscles from 11 human cadavers were dissected, the nerve entrance points located, and the dimensions measured. All muscles were stained in toto for MEPs using Acetylcholinesterase (AChE) and examined under the microscope to determine their location. Single muscle fibers were teased to evaluate the stained MEPs. RESULTS: The length of the different facial muscles varied from 29 to 65 mm, which correlated to the length of the corresponding muscle fibers. MEP zones were found on the muscles in the immediate vicinity of the nerves' entrance points and located eccentrically. Numbers and locations varied from muscle to muscle. Three MEP zone distribution patterns were differentiated: numerous small MEP zones were evenly spread over the muscle, a predominant MEP zone and two to three small zones were spread at random, and two to four MEP zones of equal size were randomly scattered. One MEP of the "en plaque" type was found in 73.8% of the muscle fibers and two to five MEPs were found in 26.2%. The distances between the multiple MEPs on one muscle fiber varied from 10 to 500 microm. CONCLUSIONS: This study suggests that facial muscles differ from skeletal muscles regarding distribution and number of MEPs. The eccentric location of MEP zones and multiple MEPs suggests there is an independent mechanism of neural regulation in the facial muscle system.

Acetylcholinesterase↗
PubMed1985

Reversal of paralysis in nerve-muscle preparations isolated from animals with hereditary motor endplate disease.

Motor endplate disease (med) in the mouse is an hereditary disorder of the skeletal neuromuscular system. Affected animals suffer a 'functional denervation' of skeletal muscle (Duchen & Stefani, 1971). Muscle fibres do not respond to indirect excitation, but motor nerve terminals release transmitter spontaneously. Spontaneous transmitter release can be enhanced by raising [K+]o or by exposing muscles to red-back spider venom and functional transmission following indirect stimulation may be restored by 4-aminopyridine.

4-Aminopyridine↗
PubMed1973

A linear dose-response curve at the motor endplate.

The motor endplate of frog sartorius muscle was voltage clamped and the peak current to different concentrations of acetylcholine and carbachol applied in the perfusing fluid was measured. Perfusing fluid was hypertonic in order to suppress contractions. Current responses were smooth and reached a peak value within 2-5 s. The dose-response curve was usually linear even with concentrations of 10(-2) M acetylcholine, indicating that the conductance change was probably proportional to the concentration of acetylcholine or carbachol. With high concentrations nonlinearity sometimes appeared but in these cases the fast onset of desensitization appeared to be preventing the current response from reaching its expected peak amplitude. When the depolarization produced by acetylcholine in a non-voltage-clamped endplate was measured the dose-response curve was hyperbolic. This relationship was imposed by the electrical properties of the endplate membrane and its surrounding sarcolemma, and could be predicted if the input resistance of the fiber was known. Experiments were also done on slow muscle fibers. Depolarizing analogues of acetylcholine had similar effects to acetylcholine. d-Tubocurarine reduced the proportionality constant between concentration of acetylcholine and conductance change, and this resulted in a parallel shift of the log-concentration depolarization curve. A linear dose-response curve was unexpected within the context of current theories of drug action.

Acetylcholine↗
PubMed2006

[Acidic fibroblast growth factor for preventing motor endplate degeneration and muscular atrophy after motor nerve injury: a morphological and electrophysiological study].

OBJECTIVE: To explore measures to prevent motor endplate degeneration and muscular atrophy after motor nerve injury. METHODS: Thirty Sprague-Dawley rats were randomized into 3 equal groups. In two of the groups, the right common peroneal nerves of the rats were transected and immediately sutured with implantation of collagen gel carrier of acidic fibroblast growth factor (aFGF) or the empty carrier into the denervated tibialis anterior muscles. In the control group, the transected nerves were sutured without implantation. Six weeks after the operation, morphological and electrophysiological examinations were performed. RESULTS: In the control rats and those with empty collagen gel carrier implantation, obvious motor endplate degeneration and muscular atrophy occurred, which were not obvious in rats receiving aFGF carrier implantation. The decrement of repetitive nerve stimulation was significantly greater in the former two groups than in the latter. CONCLUSION: Implantation of collagen gel carrier of aFGF may prevent motor endplate degeneration and facilitate functional recovery of the neuromuscular junction after motor nerve injury.

Animals↗
PubMed2001

Do endplate noise and spikes arise from normal motor endplates?

The concept that the endplate noise and endplate spike components of motor endplate potentials represent normal endplate potentials seems to be flawed. The morphology of the normal miniature endplate potentials described in the physiology literature is different from the morphology of the noise-like component of endplate potentials. This noise-like component is identified as normal in current electromyographic literature. There is strong experimental evidence that one source of the endplate noise component is grossly increased release (up to three orders of magnitude) of acetylcholine from the nerve terminal of that neuromuscular junction. The spikes can be accounted for by release of additional acetylcholine in response to mechanical stimulation by the electromyographic needle. Other possibilities exist.

Action Potentials↗
PubMed2005

Three-dimensional topography of the motor endplates of the rat gastrocnemius muscle.

Spatial distribution of motor endplates affects the shape of the electrical activity recorded from muscle. In order to provide information for realistic models of action potential propagation within muscles, we assembled three-dimensional maps of the motor endplates of the rat medial gastrocnemius (MGM) and lateral gastrocnemius (MGL) muscles. The maps were assembled from histological cross sections stained for acetylcholinesterase activity. Within MGL, the motor endplates formed three columns along its longitudinal axis. Within MGM, the motor endplates were arranged in a leaf-like body that shifted obliquely from proximal to distal. As inferred from the proximo-distal distribution of the cross-sectional projection area, the majority of the motor endplates were concentrated in the middle of MGL and in the distal third of MGM. Regions of maximal motor endplate concentration are considered most suitable for injections of neuroactive substances, such as neuronal tracers. The assembled maps of the gastrocnemius muscles can be used as guides for such injections within the motor endplate zones.

Acetylcholine↗
PubMed1982

Inhibition of human motor endplate cholinesterase by anticholinesterase compounds.

The inhibition of human motor endplate cholinesterase by anticholinesterase compounds was studied using isolated muscle membrane preparation. Ambenonium was most potent, and edrophonium was least potent in inhibiting motor endplate cholinesterase. The slope of the regression line for inhibition of motor endplate cholinesterase was greatest for ambenonium, and smallest for neostigmine and edrophonium. These compounds were less potent inhibitors of plasma cholinesterase. Ambenonium was more specific, and other compounds were less specific inhibitors of motor endplate cholinesterase. In myasthenic patients, these compounds produced adequate inhibition of motor endplate cholinesterase even in the presence of relatively mild plasma cholinesterase inhibition.

Cholinesterase Inhibitors↗
PubMed1982

Electrophysiological and morphological studies of a motor nerve in 'motor endplate disease' of the mouse.

Motor nerves of mice affected with hereditary 'motor endplate disease' were examined by means of electrophysiological and morphological techniques. Conduction velocity was slower, the refractory period was prolonged and the temperature sensitivity higher in mutants as compared to controls of the same age. Most of the axons examined in the electron microscope showed signs of paranodal demyelination. The relationship between the morphological and the electrophysiological findings is discussed. We conclude that alterations in the motor axons can account for the failures in neuromuscular transmission described previously in the med mutation.

Animals↗
PubMed1979

Attachment of acetylcholinesterase to structures of the motor endplate.

The kinetics of AChE solubilization from intact motor endplates of mouse diaphragm, by collagenase, papain and hyaluronidase, was studied in parallel with the ultrastructural localization of AChE in treated neuromuscular junctions. Hyaluronidase did not solubilize more AChE from isolated motor endplate regions than Ringer's solution itself. Residual AChE activity could be demonstrated histochemically in motor endplates even after the plateau of solubilization by collagenase or papain was reached. Less than 35% of junctional AChE is left after collagenase, and less than 20% after papain treatment, as estimated by the percentage of AChE activity left in the isolated endplate region of the diaphragm after protease treatment. Cytochemically, both proteases had a similar effect on postsynaptic AChE. Residual AChE activity was distributed randomly, adhering to the sarcolemma of junctional clefts. Presynaptic AChE localized in the gap between axon terminal and Schwann cell appears to be resistant to collagenase but not to papain treatment. The mode of AChE attachment or the composition of the intercellular material in this gap may differ from that of the primary and secondary clefts.

Acetylcholinesterase↗
PubMed2004

Evoked pain in the motor endplate region of the brachial biceps muscle: an experimental study.

Spontaneous electrical activity, interpreted as motor endplate activity, has been reported at muscle trigger points. This study examined whether the motor endplate region, identified by electromyography, is more sensitive to noxious stimuli than other muscle sites. We induced pain in the brachial biceps muscles of 21 healthy subjects by injecting capsaicin (30 microg/0.1 ml) and NaCl (5%/0.2 ml) in the motor endplate region and at electrically silent muscle sites. Needle and evoked pain were measured by a visual analogue scale (VAS) (0-10) and the short form of the McGill Pain Questionnaire. The needle pain in the motor endplate region differed both in intensity and quality from that at other sites. The maximal pain after NaCl 5% was higher, and the VAS area-under-the-curve for NaCl 5% and capsaicin were larger, in the motor endplate region than in other sites. A higher density of muscle nociceptors in the vicinity of the motor endplate region may account for the observed differences in pain. These findings may have clinical implications for the treatment of musculoskeletal pain conditions.

Adult↗
PubMed1988

Structure of motor endplates in the different fiber types of vertebrate skeletal muscles.

The number and localization of vertebrate motor endplates on the muscle fiber, and their structure, vary according to phylum and species, and among the different fiber types in a given species. Vertebrate skeletal muscle fibers are classified into two major groups: the twitch (fast) and the slow (tonic) fibers. The twitch fiber has straight Z-lines and a well developed T-SR system, and is singly innervated with en plaque (plate-like) type motor endplate. The twitch fibers are further subdivided into three types: the red (mitochondria-rich), intermediate (mitochondria-moderate) and white (mitochondria-poor) fibers. The motor endplate of the white fiber is large and has a complicated structure, that of the red fiber is small and less complicated, and that of the intermediate fiber possesses intermediate characteristics. The slow fiber has zigzag Z-lines and poorly developed sarcoplasmic reticulum (SR), and is multiply innervated with en grappe (grape-like) type motor endplates. The morphological features of the motor endplate in each of these fiber types of the mammalian, avian, reptilian, amphibian, and fish skeletal muscles are reviewed. Special emphasis has been placed on the three-dimensional structure of the motor endplates of the different fiber types as observed by high-resolution scanning electron microscopy.

Amphibians↗
PubMed1991

Compartmentalized transcription of acetylcholine receptor genes during motor endplate epigenesis.

In the adult motor endplate the acetylcholine receptor protein (AChR) is strictly localized under the motor nerve ending, whereas in the noninnervated myotube it is distributed all over the surface of the cell. The genesis of this anisotropic distribution involves a differential regulation of AChR gene transcription. In situ hybridization with AChR subunit probes discloses high levels of unspliced and mature mRNA all over differentiating myotubes. After the entry of the exploratory motor axons, the mRNA clusters located outside the endplate decrease in number and become restricted to the subneural "fundamental" nuclei. Denervation causes a reappearance of unspliced and mature mRNA in extrajunctional areas. A compartmentalized expression of AChR genes take place during endplate formation. Chronic paralysis of the embryo interferes with the disappearance of extrajunctional AChR that, thus, represents an electrical activity-dependent repression of AChR genes. The entry of Ca2+ ions through the sarcolemmal membrane during electrical activity and the activation of protein kinase C plausibly contribute to this membrane-to-gene regulation. The maintenance and late increase in AChR number at the endplate requires the intervention of an anterograde signal or signals, of neural origin. Several factors have been suggested to play a role in this process, such as an acetylcholine receptor-inducing activity (ARIA), ascorbic acid, or calcitonin gene-related peptide (CGRP), a peptide known to coexist with acetylcholine in spinal cord motoneurons. In cultured chick muscle cells, CGRP increases the concentration of surface AChR and alpha-subunit unspliced and mature mRNA and stimulates membrane-bound adenylate cyclase, suggesting that distinct second messengers are involved in the regulation of AChR biosynthesis by electrical activity and by CGRP. The data are interpreted in terms of a model in which it is assumed that (i) in the adult muscle fiber, different stages of gene expression occur in the nuclei in subneural and extrajunctional areas, and (ii) different second messengers elicited by neural factors or electrical activity regulate the state of transcription of these nuclei via trans-acting allosteric proteins binding to cis-acting DNA regulatory elements. The upstream flanking regions of several of the AChR subunit genes reveal ubiquitous DNA elements such as TATA and CAAT boxes, Sp1 binding sites and SV40 core enhancer sites, and muscle-specific MyoD (CANNTG) elements. The contribution of some of these elements to the differential regulation of the multiple AChR subunits is discussed.

Animals↗
PubMedDate not supplied

Morphological features of nerve terminal degeneration as part of the remodeling process in the motor endplate in adult muscles.

With the exception of signs of retraction and withdrawal, there have been few morphological data concerning degenerated neural profiles in adult motor endplates. Here, investigation into the ultrastructure of the soleus motor endplates of adult rats (4 months old) turned up particular axonal degeneration in approximately 3% of the subjects. These axons occur as synaptic debris in the synaptic matrix of the motor endplate, adjacent to thin processes of the perisynaptic cells occupying the outermost layer of the motor endplate and were devoid of basal lamina. They often possessed dense-cored vesicles (50-80 nm). Axonal debris released from Schwann cell processes occurred during the period of acute sciatic neurectomy, when nerve terminals progressively disrupted within the motor endplate-associated Schwann cells. Finally, immunohistochemical staining for antibodies to label macrophages (ED1 or ED2) has shown that nerve fiber-associated macrophages are located near the motor endplate. The results suggest that during the course of endplate remodeling, a few parts of the terminal branches are disposed of through spontaneous collapse, subsequent release from the Schwann cell investment, and eventual ingestion by macrophages in the perisynaptic space.

Animals↗
PubMed1985

The three-dimensional structure of motor endplates in different fiber types of rat intercostal muscle. A scanning electron-microscopic study.

The three-dimensional organization of the motor end plates in the red, white and intermediate striated muscle fibers of the rat intercostal muscle was observed under a field-emission type scanning electron microscope after removal of connective tissue components by HCl hydrolysis. The motor endplate of the white fiber had terminal branches (or axon terminals), which were large, long and thin, and small but numerous nerve swellings (or terminal boutons). The motor endplate of the red fiber had terminal branches, which were small, short and thick, and had large but fewer nerve swellings. The motor endplate of the intermediate fiber was intermediate in size and structure between these two. In detached nerve-ending preparations, primary synaptic grooves with slit-like openings of the junctional folds appeared on the surface of the muscle fibers. The primary synaptic grooves were more developed in the white fiber than in the red fiber, and they were intermediate in the intermediate fiber. The numerical ratio of slit-like openings was 1:1.8:3.5 in the red, intermediate and white fiber, respectively. The Schwann cells and their processes were observed on the surface of the motor endplate, with the processes covering the upper orifices of the primary synaptic grooves and sealing the terminal branches. The number of Schwann cells was usually three in the white fiber, two in the intermediate fiber and one in the red fiber.

Animals↗
PubMed1995

Mutation of a new sodium channel gene, Scn8a, in the mouse mutant 'motor endplate disease'.

The mouse neurological mutant 'motor endplate disease' (med) is characterized by early onset progressive paralysis of the hind limbs, severe muscle atrophy, degeneration of Purkinje cells and juvenile lethality. We have isolated a voltage-gated sodium channel gene, Scn8a, from the flanking region of a transgene-induced allele of med. Scn8a is expressed in brain and spinal cord but not in skeletal muscle or heart, and encodes a predicted protein of 1,732 amino acids. An intragenic deletion at the transgene insertion site results in loss of expression. Scn8a is closely related to other sodium channel alpha subunits, with greatest similarity to a brain transcript from the pufferfish Fugu rubripes. The human homologue, SCN8A, maps to chromosome 12q13 and is a candidate gene for inherited neurodegenerative disease.

Amino Acid Sequence↗
PubMed1996

Acetylcholine release at motor endplates and autonomic neuroeffector junctions: a comparison.

Acetylcholine released at motor endplates and at autonomic neuroeffector junctions binds to nicotinic and muscarinic receptors to affect the activity of the corresponding target cells. Additionally, nicotonic and muscarinic receptors modulate various intracellular regulatory pathways (second messengers, gene expression) and mediate trophic effects. To maintain homeostasis of the individual cell and of the whole organism the release of acetylcholine has to be strictly controlled within both nervous systems. The basic events of synthesis, storage, and release are comparable at motoneurones and autonomic neurones, but mechanisms regulating transmitter release appear to differ. The motor endplate can be regarded as a highly specialized synapse ensuring a focal innervation of skeletal muscle fibres. P-type calcium channels are critically involved in mediating exocytotic transmitter release. Facilitatory presynaptic receptors (nicotinic, muscarinic, alpha 1- and beta 1-adrenoceptors, calcitonin-gene-related peptide receptors, adenosine A2a receptors) mediate an increase in evoked acetylcholine release to allow rapid and maximal activation of skeletal muscles. In contrast, neuroeffector junctions innervate the effector cells in a rather scattered manner. N-type calcium channels are critically involved in exocytotic transmitter release. Inhibitory neuronal receptors (muscarinic, alpha 2- and beta-adrenoceptors, prostanoid (airways), receptors for NO, P1-purinoceptors) limit evoked acetylcholine release to prevent overstimulation of the effector cells. These inhibitory mechanisms may also be useful in view of the 100-fold higher affinity of acetylcholine at muscarinic receptors than at nicotinic receptors (muscular type), a property which may facilitate overstimulation.

Acetylcholine↗
PubMed1983

Intense ultraterminal sprouting from motor nerves and ultrastructural aspects of the neuromuscular junction and non-junctional sarcolemma of the soleus (slow-twitch) muscle in motor endplate disease in the mouse.

Motor end-plate disease (med) in the mouse is an hereditary defect of the neuromuscular system, with partial functional denervation and muscle inactivity in late stages of the disease. Motor end-plate disease is characterized by an intense ultraterminal sprouting of the motor nerves from swollen nerve terminal branches in the soleus muscle. At the ultrastructural level, the neuromuscular junctions extend to very wide territories, often outside the original motor end-plate, in regions where the nerve sprouts are in simple apposition to the muscle fiber, with no secondary synaptic folds. The nerve terminals are rich in neurofilaments and poor in synaptic vesicles. Freeze fracture analysis of the pre-synaptic and post-synaptic membrane specializations fails to reveal any important structural alteration which could suggest a defect in acetylcholine release or in muscle membrane excitability. However, the non-junctional sarcolemmal specializations (the so-called 'square arrays') are found with a frequency slightly higher than in normal muscle. The nerve abnormalities at the neuromuscular junction may be either a consequence of muscle inactivity or the morphological expression of some primary nerve abnormality. Further studies of the soleus muscle at early stages of the disease may provide evidence in favor of either possibility.

Animals↗