The effect of partial denervation of developing rats fast muscles on their motor unit properties.

Tyč, F.; Vrbová, Gerta

doi:10.1113/jphysiol.1995.sp020547

Cited by 19 publications

(8 citation statements)

References 18 publications

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“…The 2-week recovery interval was deliberately chosen because it leaves insufficient time for effective reinnervation of those fibers by collateral or nodal sprouting from remaining, intact motor axons but still is long enough to allow upregulation of NCAM in denervated muscle fibers. 1,19,34 NCAM is a cell-surface glycoprotein that is abundant along the sarcolemma of embryologic, fetal, and postnatal skeletal muscle. With innervation, NCAM becomes colocalized with the acetylcholine receptor at the neuromuscular junction and is limited to this location in adult muscle.…”

Section: Discussionmentioning

confidence: 99%

A specific force deficit exists in skeletal muscle after partial denervation

et al. 2001

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Skeletal muscle demonstrates a specific force deficit after repair of injured peripheral nerves, microneurovascular muscle transfer, and normal aging. Because atrophy cannot account for deficits in specific force, other, unknown, mechanisms are responsible for the resulting muscle contractile dysfunction under these circumstances. We tested the hypothesis that a subpopulation of denervated fibers is partially or completely responsible for the specific force deficit after partial denervation of the rat extensor digitorum longus muscle (EDL). Adult Fisher rats underwent either sham exposure or partial transection of 80% of the cross-sectional area of the left deep peroneal nerve. After a 2-week recovery period, maximum isometric force (F(0)) was measured in situ and maximum specific force (sF(0)) was calculated for EDL from both control (n = 8) and partial denervation (n = 7) groups. Innervated fiber cross-sectional area (CSA(inn)) was measured directly from whole EDL cross sections after immunohistochemical labeling for neural cell adhesion molecule (NCAM), a marker of muscle fiber denervation. A corrected specific force value (sF(0-inn)) was calculated by normalizing F(0) to CSA(inn). Partial skeletal muscle denervation resulted in significant reductions in muscle mass, F(0), and sF(0). The percentage of muscle fibers expressing NCAM in the extrajunctional sarcolemma increased from 1.0 +/- 0.8% in control to 49 +/- 15% in partially denervated EDL muscles. A 62.7% deficit in EDL specific force was observed after partial denervation. Denervated muscle fibers accounted for 59.3% of this deficit, but sF(0-inn) still differed significantly between control and partially denervated muscles, with a 25.5% difference between groups. In partially denervated muscles, the specific force deficit is partially but not fully explained by a subpopulation of noncontractile, denervated fibers.

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Section: Discussionmentioning

confidence: 99%

A specific force deficit exists in skeletal muscle after partial denervation

et al. 2001

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“…Since that time, several lines of evidence have developed showing that denervation occurs in aging muscles, including a progressive reduction in the number of motoneurons in the spinal cord beginning at ≈60 y [5], loss of motoneurons in the periphery [6], [7], fiber type grouping [8], [9], degeneration of neuromuscular junctions [4], [10], loss of motor units [11], [12], and grouped fiber atrophy in aging muscle [13], [14]. It is also striking that the muscle morphological alterations in aging human muscle, e.g., accumulation of severely atrophic angular fibers [14], [15], [16], are similar to those seen in motoneuron diseases and in experimental models of denervation [17], [18], [19]. Finally, some fibers in aged muscles express markers of denervation, such as neural cell adhesion molecule [20] and the sodium channel, Nav 1.5 [21].…”

Section: Introductionmentioning

confidence: 99%

Denervation Causes Fiber Atrophy and Myosin Heavy Chain Co-Expression in Senescent Skeletal Muscle

et al. 2012

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Although denervation has long been implicated in aging muscle, the degree to which it is causes the fiber atrophy seen in aging muscle is unknown. To address this question, we quantified motoneuron soma counts in the lumbar spinal cord using choline acetyl transferase immunhistochemistry and quantified the size of denervated versus innervated muscle fibers in the gastrocnemius muscle using the in situ expression of the denervation-specific sodium channel, Nav1.5, in young adult (YA) and senescent (SEN) rats. To gain insights into the mechanisms driving myofiber atrophy, we also examined the myofiber expression of the two primary ubiquitin ligases necessary for muscle atrophy (MAFbx, MuRF1). MN soma number in lumbar spinal cord declined 27% between YA (638±34 MNs×mm−1) and SEN (469±13 MNs×mm−1). Nav1.5 positive fibers (1548±70 μm2) were 35% smaller than Nav1.5 negative fibers (2367±78 μm2; P<0.05) in SEN muscle, whereas Nav1.5 negative fibers in SEN were only 7% smaller than fibers in YA (2553±33 μm2; P<0.05) where no Nav1.5 labeling was seen, suggesting denervation is the primary cause of aging myofiber atrophy. Nav1.5 positive fibers had higher levels of MAFbx and MuRF1 (P<0.05), consistent with involvement of the proteasome proteolytic pathway in the atrophy of denervated muscle fibers in aging muscle. In summary, our study provides the first quantitative assessment of the contribution of denervation to myofiber atrophy in aging muscle, suggesting it explains the majority of the atrophy we observed. This striking result suggests a renewed focus should be placed on denervation in seeking understanding of the causes of and treatments for aging muscle atrophy.

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“…In contrast, a decrease in fatigability has been reported for the extensor digitorum longus muscle after full (Lowrie et al, 1990) or partial (Tyc and Vrbová, 1995) denervation in early postnatal development (P3-P18). These authors also report decreased TPT, increased HRT, and higher numbers of slow fibers after neonatal denervation and reinnervation (Tyc and Vrbová, 1995), changes that were more pronounced in muscles denervated on P3 than P18. The decreased fatigability in these studies, therefore, may be due in part to either a conversion of fibers from fast to slow or a selective sparing of slow twitch fibers.…”

Section: Increased Fatigability Of the Reinnervated La Musclementioning

confidence: 91%

Reinnervation of the rat levator ani muscle after neonatal denervation

Lubischer¹,

Unguez²,

Pierotti³

et al. 2005

J. Neurobiol.

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After axonal injury on postnatal day 14 (P14), but not P21, motoneurons in the spinal nucleus of the bulbocavernosus (SNB) do not display their normal response to circulating testosterone levels. This could result from a permanent disruption of communication between motoneurons and their testosterone-sensitive target muscles. We assessed the extent of reinnervation of one of these target muscles, the levator ani (LA) muscle, 5 months after the pudendal nerve was cut either on P14 or P21. The number of motoneurons innervating the LA in control and nerve cut animals was determined using retrograde labeling procedures. Functional recovery of the LA muscle was determined via the testing of its in situ contractile properties. Compared to control muscles, reinnervated LA muscles were smaller, had fewer muscle fibers, generated a lower maximum tetanic tension, and were more fatigable. In spite of the fact that fewer motoneurons reinnervated the LA muscle after nerve cut on P14 than on P21, there were no differences in the weight or contractile properties of the LA muscle between these two groups. These data suggest that motoneurons that survived injury on P14 innervated more muscle fibers than normal and exhibited a similar ability to functionally reinnervate the target muscle as those motoneurons that survived injury on P21.

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The effect of partial denervation of developing rats fast muscles on their motor unit properties.

Cited by 19 publications

References 18 publications

A specific force deficit exists in skeletal muscle after partial denervation

A specific force deficit exists in skeletal muscle after partial denervation

Denervation Causes Fiber Atrophy and Myosin Heavy Chain Co-Expression in Senescent Skeletal Muscle

Reinnervation of the rat levator ani muscle after neonatal denervation

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