Morphological changes in the human end plate with age

Wokke, John H. J.; Jennekens, F. G. I.; Oord, C.J.M. van den; Veldman, H.; Smit, L. M. E.; Leppink, G.J.

doi:10.1016/0022-510x(90)90076-y

Cited by 111 publications

(90 citation statements)

References 39 publications

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“…Former studies by other authors concerning the innervation of human skeletal muscles (Desmedt, 1958;Christensen, 1959;Schwarzacher, 1959;Aquilonius et al, 1984;Carlson, 1986;Wokke et al, 1990;Hesselmans et al, 1993) have shown that focal innervation of muscle fibers with one MEP is the predominant type. We conclude that multifocally innervated fibers would have been found by these authors if present.…”

Section: Discussionmentioning

confidence: 96%

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

et al. 1997

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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 µm.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. Anat.

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Section: Discussionmentioning

confidence: 96%

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

et al. 1997

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“…Aged rats may compensate for this AChR loss by changes in threshold endplate potentials (safety factors) or by increasing their quantal release more efficiently to compensate for the decreased postsynaptic sensitivity resulting from AChR loss [42]. Moreover, differences in susceptibility might be explained by changes at the endplate in aged rats, such as increased length and branching of the postsynaptic membrane and enlargement of the postsynaptic area, or wider spacing of the AChR molecules [43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

Age- and sex-related resistance to chronic experimental autoimmune myasthenia gravis (EAMG) in Brown Norway rats

Hoedemaekers¹,

Graus²,

Vriesman³

et al. 1997

Clinical and Experimental Immunology

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SUMMARYThe influence of age and sex on the induction of chronic EAMG was analysed. Aged male rats, immunized with Torpedo acetylcholine receptor (tAChR), showed no clinical signs of disease or AChR loss. Immunization of young male Brown Norway (BN) rats resulted in both clinical signs of disease and 65% AChR loss. In contrast, both young and aged female BN rats showed comparable AChR loss (58% and 50%, respectively), although aged female rats did not develop clinical signs of disease. Differences in antibody titres, isotype distribution, fine specificity or complement activation could not account for the observed resistance. These results suggest that resistance against EAMG in aged rats is due to resistance of the AChR against antibody-mediated degradation, or to mechanisms able to compensate for AChR loss.

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“…In contrast, skeletal neuromuscular junctions (NMJs) are ideal for analysis of synaptic architecture: they are highly accessible, relatively simple, functionally uniform, and so much larger than central synapses that their size and shape can be assessed light microscopically (11). Moreover, several studies have noted differences in neuromuscular structure between young adult and aged rodents (12)(13)(14)(15)(16) and humans (17,18). Here, we characterized and quantified these changes and determined their time course using transgenic mice in which motor axons were indelibly labeled with fluorescent proteins (19).…”

mentioning

confidence: 99%

Attenuation of age-related changes in mouse neuromuscular synapses by caloric restriction and exercise

Valdez

Tapia

Kang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

438

540

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The cellular basis of age-related behavioral decline remains obscure but alterations in synapses are likely candidates. Accordingly, the beneficial effects on neural function of caloric restriction and exercise, which are among the most effective anti-aging treatments known, might also be mediated by synapses. As a starting point in testing these ideas, we studied the skeletal neuromuscular junction (NMJ), a large, accessible peripheral synapse. Comparison of NMJs in young adult and aged mice revealed a variety of age-related structural alterations, including axonal swellings, sprouting, synaptic detachment, partial or complete withdrawal of axons from some postsynaptic sites, and fragmentation of the postsynaptic specialization. Alterations were significant by 18 mo of age and severe by 24 mo. A life-long calorie-restricted diet significantly decreased the incidence of pre-and postsynaptic abnormalities in 24-mo-old mice and attenuated age-related loss of motor neurons and turnover of muscle fibers. One month of exercise (wheel running) in 22-mo-old mice also reduced age-related synaptic changes but had no effect on motor neuron number or muscle fiber turnover. Time-lapse imaging in vivo revealed that exercise partially reversed synaptic alterations that had already occurred. These results demonstrate a critical effect of aging on synaptic structure and provide evidence that interventions capable of extending health span and lifespan can partially reverse these age-related synaptic changes.aging | neuromuscular junction | muscle | motor neuron | sarcopenia A ging is accompanied by numerous functional alterations of both the central and peripheral nervous systems (1). Until recently, it was thought that many of these age-associated changes were secondary to neuronal degeneration. Recent studies show, however, that little neuronal death occurs in most areas of the aging nervous system (2). Although many possible explanations exist (3-6), a particularly attractive hypothesis is that some agerelated alterations in mental function result from synaptic alterations. Supporting this idea, alterations in synapse number, spine densities, and synaptic plasticity have been documented in the brains of aging humans and experimental animals (1,7,8).If synaptic changes underlie age-related defects in neural function, one might look to synapses as targets for treatments that minimize the decline. Two lifestyle regimens that have been consistently demonstrated to extend lifespan and mitigate agerelated changes in neural function are caloric restriction and exercise (9). In that the cellular bases of age-related changes in mental activity are obscure, it is not surprising that the means by which exercise and caloric restriction attenuate these changes are also unknown. For both regimens, however, synaptic alterations have figured prominently among proposed mechanisms (9, 10).An obstacle to progress in this area is the complexity and diversity of synaptic neuropil in the brain, which impedes detailed analysis of aging central syna...

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Morphological changes in the human end plate with age

Cited by 111 publications

References 39 publications

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

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

Age- and sex-related resistance to chronic experimental autoimmune myasthenia gravis (EAMG) in Brown Norway rats

Attenuation of age-related changes in mouse neuromuscular synapses by caloric restriction and exercise

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