Evidence of schwann cell degeneration in the aging mouse motor end-plate region

Ludatscher, Ruth M.; Silbermann, Michael; Gershon, David; Reznick, Abraham Z.

doi:10.1016/0531-5565(85)90043-9

Cited by 17 publications

(14 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…With progressive age, we noted decreased tSC numbers at the WT NMJ, with abnormalities in tSC contour, staining, and cytoplasmic processes. Our tSC data corroborate with those of others (Boaro et al., 1998; Chai et al., 2011; Kawabuchi et al., 2001; Ludatscher, Silbermann, Gershon & Reznick, 1985). By 27 months of age, tSC degeneration was noted in 35% of NMJs in mouse gastrocnemius in contrast to the absence of tSC degenerative changes in 6‐month‐old mice (Ludatscher et al., 1985).…”

Section: Discussionmentioning

confidence: 99%

“…Our tSC data corroborate with those of others (Boaro et al., 1998; Chai et al., 2011; Kawabuchi et al., 2001; Ludatscher, Silbermann, Gershon & Reznick, 1985). By 27 months of age, tSC degeneration was noted in 35% of NMJs in mouse gastrocnemius in contrast to the absence of tSC degenerative changes in 6‐month‐old mice (Ludatscher et al., 1985). Additionally, tSCs have been noted to be thin, disorganized, and to only partially cover the endplates in advanced aged mice (Chai et al., 2011; Kawabuchi et al., 2001), similar to the tSC changes we noted in the DMH‐specific Sirt1 knockdown mice in this study.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hypothalamic Sirt1 protects terminal Schwann cells and neuromuscular junctions from age‐related morphological changes

et al. 2018

View full text Add to dashboard Cite

SummaryNeuromuscular decline occurs with aging. The neuromuscular junction (NMJ), the interface between motor nerve and muscle, also undergoes age‐related changes. Aging effects on the NMJ components—motor nerve terminal, acetylcholine receptors (AChRs), and nonmyelinating terminal Schwann cells (tSCs)—have not been comprehensively evaluated. Sirtuins delay mammalian aging and increase longevity. Increased hypothalamic Sirt1 expression results in more youthful physiology, but the relationship between NMJ morphology and hypothalamic Sirt1 was previously unknown. In wild‐type mice, all NMJ components showed age‐associated morphological changes with ~80% of NMJs displaying abnormalities by 17 months of age. Aged mice with brain‐specific Sirt1 overexpression (BRASTO) had more youthful NMJ morphologic features compared to controls with increased tSC numbers, increased NMJ innervation, and increased numbers of normal AChRs. Sympathetic NMJ innervation was increased in BRASTO mice. In contrast, hypothalamic‐specific Sirt1 knockdown led to tSC abnormalities, decreased tSC numbers, and more denervated endplates compared to controls. Our data suggest that hypothalamic Sirt1 functions to protect NMJs in skeletal muscle from age‐related changes via sympathetic innervation.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hypothalamic Sirt1 protects terminal Schwann cells and neuromuscular junctions from age‐related morphological changes

et al. 2018

View full text Add to dashboard Cite

show abstract

“…However, such changes in SCs will have an adverse effect on the maintenance of the remaining NMJ and possible re-innervation. Most studies have examined alterations in SCs after nerve crush or transection [44], whereas very few have examined SCs in ageing muscles [45], [46]. An electron microscopic study of gastrocnemius muscles in mice showed no SC degeneration in young adults (6 months) but degeneration of SCs and their processes in 35% of the NMJs at 27 months [45].…”

Section: Discussionmentioning

confidence: 99%

Striking Denervation of Neuromuscular Junctions without Lumbar Motoneuron Loss in Geriatric Mouse Muscle

et al. 2011

View full text Add to dashboard Cite

Reasons for the progressive age-related loss of skeletal muscle mass and function, namely sarcopenia, are complex. Few studies describe sarcopenia in mice, although this species is the mammalian model of choice for genetic intervention and development of pharmaceutical interventions for muscle degeneration. One factor, important to sarcopenia-associated neuromuscular change, is myofibre denervation. Here we describe the morphology of the neuromuscular compartment in young (3 month) compared to geriatric (29 month) old female C57Bl/6J mice. There was no significant difference in the size or number of motoneuron cell bodies at the lumbar level (L1–L5) of the spinal cord at 3 and 29 months. However, in geriatric mice, there was a striking increase (by ∼2.5 fold) in the percentage of fully denervated neuromuscular junctions (NMJs) and associated deterioration of Schwann cells in fast extensor digitorum longus (EDL), but not in slow soleus muscles. There were also distinct changes in myofibre composition of lower limb muscles (tibialis anterior (TA) and soleus) with a shift at 29 months to a faster phenotype in fast TA muscle and to a slower phenotype in slow soleus muscle. Overall, we demonstrate complex changes at the NMJ and muscle levels in geriatric mice that occur despite the maintenance of motoneuron cell bodies in the spinal cord. The challenge is to identify which components of the neuromuscular system are primarily responsible for the marked changes within the NMJ and muscle, in order to selectively target future interventions to reduce sarcopenia.

show abstract

“…The most interesting finding, which was not observed in young animals, was the appearance of degenerated Schwann cells in the endplates of the old mice. Overall, while the young group had, in proportion, 85% of the normally structured endplates, this number was reduced to 40% in the old group (72).…”

Section: Control By the Central Nervous System (Cns)mentioning

confidence: 97%

The Physiology and Biochemistry of Skeletal Muscle Atrophy as a Function of Age

Carmeli¹,

Reznick²

1994

Experimental Biology and Medicine

View full text Add to dashboard Cite

The skeletal muscles are an important entity in the proper function of aging animals and humans. Studies have shown that until humans are 60-70 years old, age-related changes in muscle function and structure are relatively small, while after 70 years, these alterations are accelerated considerably. Factors responsible for the "aging" of skeletal muscles are complex and include intrinsic biochemical changes in muscle metabolism, changes in the distribution and size of muscle fibers, and a general loss of muscle mass. In addition, other factors like the control of muscle contraction by the motor neural system and the influence of external conditions such as exercise, immobility, nutrition and others may also contribute to the age-related decrease in muscle functions. Studies have shown that with age there is some loss of peripheral motor neurons, reduction in the number of motor units, alterations in the neuromuscular junctions, and selective denervation of Type II muscle fibers. These findings led to the concept of denervation atrophy of skeletal muscles as one of the major mechanisms for muscle degeneration in old age. However, it should be emphasized that the extent of age-related changes varies from muscle to muscle, and some do not seem to be affected by age. For example, it has been shown recently, in animal studies, that weight-bearing muscles are much more susceptible to senescent processes than non-weight-bearing muscles. More work is needed to clarify the contributions of the various factors, especially the role of muscle training in alleviating the symptoms of age-related muscle atrophy.

show abstract

Evidence of schwann cell degeneration in the aging mouse motor end-plate region

Cited by 17 publications

References 22 publications

Hypothalamic Sirt1 protects terminal Schwann cells and neuromuscular junctions from age‐related morphological changes

Hypothalamic Sirt1 protects terminal Schwann cells and neuromuscular junctions from age‐related morphological changes

Striking Denervation of Neuromuscular Junctions without Lumbar Motoneuron Loss in Geriatric Mouse Muscle

The Physiology and Biochemistry of Skeletal Muscle Atrophy as a Function of Age

Contact Info

Product

Resources

About