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1.
Membrane potentials, cable parameters, and component resting conductances were measured in extensor digitorum longus (EDL) muscle fibers from adult rats in vitro at 24°C, after 15 to 18 days of denervation by nerve section, and at seven to ten days following epineural injection of 100 to 450 μg of colchicine in the peroneal nerve. The denervated muscles were paralyzed throughout the experimental period, whereas the colchicine-treated preparations showed no clinical paralysis except for the first day or two. The EDL from the untreated side served as a control. Both the denervated and colchicine-treated fibers were depolarized, showed signs of fibrillation, had tetrodotoxin-resistant action potentials, and membrane resistance was increased two- to sevenfold. In the denervated fibers, mean chloride conductance GCl dropped from a control value of 3196 to 596 μmhos/cm2 while mean potassium conductance GK showed a tendency to rise from 260 to 332 μmhos/cm2. Colchicine-treated fibers while showing a similar fall in mean GCl from 2993 to 1066 μmhos/cm2, also showed a significant fall in mean GK from 213 to 116 μmhos/cm2. It was concluded that factors transported by the microtubular system are important for the maintenance of the high resting GCl of mammalian skeletal muscle fibers. 相似文献
2.
Membrane potentials, cable parameters, and component resting ionic conductances of gastrocnemius fibers from normal goats were measured in vitro at six to 32 days following denervation by section of the tibial nerve. Denervated fibers were depolarized an average of 11.6 ± 1.5 mV (six preparations) from the control mean of 62.1 ± 1.0 mV (124 fibers) over the period studied. Fibrillation, tetrodotoxin-resistant action potentials, and anodebreak excitation were present in the denervated preparations after 13 days. The control cable parameters from 124 fibers (13 preparations) were membrane resistance, 1052 ± 70 ω·cm2 and membrane capacitance, 6.2 μF/cm2. In denervated fibers membrane resistance increased two to three times in the 13 to 32 day period; membrane capacitance increased about 50% in normal solution at eight to nine, 27–28, and 32 days. Myoplasmic resistivity was assumed to be 112 Ωcm. Measurements were made at 38°C. Component resting conductances were determined from the cable parameters in normal and chloride-free solution. Mean chloride conductance GCl and mean potassium conductance GK of control fibers were 776 ± 49 μmhos/cm2 and 175 ± 15 μmhos/cm2 (92 fibers), respectively. Following denervation GCl increased slightly at six to nine days then fell to low values at 16 to 32 days that were close to or indistinguishable from zero. GK increased significantly to 372 ± 40 μmhos/cm2 and 499 ± 90 μmhos/cm2 at 16 to 20 and 32 days, respectively. It was concluded from these findings that GCl and GK of mammalian skeletal muscle are controlled by factors from the nerve and/or muscle action potentials. Goat muscle is different from frog muscle in which GCl does not change and GK decreases during denervation. 相似文献
3.
Our previous studies have shown that partial denervation of extensor digitorum longus muscle (EDL) in the rat at 3 days of age causes an increase in the activity of the intact motoneurons. The originally phasic pattern of activity of EDL became tonic after partial denervation. These modifications of motoneuron activity were associated with the change in the phenotype of the muscle from fast to slow contracting and with a conversion of the muscle fibres from a fast to a slow type. The present study investigates whether the size of the cell body of the active EDL motoneurons change in parallel with the altered muscular activity. The study involved partial denervation of rat EDL muscle by section of the L4 spinal nerve at 3 days of age. Then the remaining motoneurons from L5 spinal nerve supplying the EDL muscle were retrogradly labelled with horseradish peroxidase two months later. The results show a reduction in motoneuron size in parallel with an increase in activity of the motoneurons after partial denervation of EDL muscle. 相似文献
4.
Summary Changes of muscle weights, fiber diameters and ultrastructure were studied in the slow anterior latissimus dorsi (ALD) and in the fast posterior latissimus dorsi (PLD) of the chick three weeks after denervation and tenotomy, and after combined denervation and tenotomy of the two muscles.The slow ALD muscle becomes hypertrophic after denervation (Feng, Jung and Wu, 1962). Three weeks after nerve section, wet weights of ALD muscles are increased by 60% and fiber diameters become by 30% larger than those of contralateral control muscles. In spite of this hypertrophy, degenerative changes are seen in the ultrastructure, similar to those described in denervated atrophic muscles. Areas of dedifferentiation with autophagic vacuoles and aggregates of tubules are found in superficial layers of some fibers. Disintegration of Z lines and filaments along one or two sarcomeres occurs in a number of myofibrils, especially in muscles of young animals.In contrast to denervation alone, simultaneous denervation and tenotomy of the ALD muscles results in atrophy. Decrease of muscle weights and reduction of fiber diameters are similar as after tenotomy; in both cases muscle fibers waste by degeneration and atrophy of myofibrils.The fast PLD muscles underwent extensive atrophy in all three series of experiments. Corresponding atrophic and degenerative changes of ultrastructure were found in all instances.The authors wish to acknowledge gratefully the skillful technical assistance of Mrs. M. Sobotková and Ing. M. Doubek, and editorial assistance of Miss Virginia Hamilton. 相似文献
5.
EISENBERG BC 《California medicine》1958,88(1):33-38
Traumatic peripheral nerve lesions characteristically result in denervation muscular atrophy. Atrophy of disuse may take place concomitantly, either proximal, adjacent to or distal to the denervation muscular atrophy. The degree of atrophy of disuse depends upon the severity of the nerve lesion. Clinically, it is difficult to determine where true denervation muscular atrophy ends and accompanying atrophy of disuse begins. In such circumstances a clinician may be misled into belief that the cause of so apparently extensive a lesion is elsewhere. The patient then is often submitted to other complex diagnostic procedures and treatments. This difficulty can usually be dissipated by the use of electromyography, for each specific type of muscular atrophy produces its own characteristic electromyographic changes. Disuse atrophy produces no changes in electrical activity, whereas denervation atrophy manifests itself by typical denervation activity. Moreover it is possible to determine what part of muscular atrophy in a given area is owing to damage to a nerve and what part is owing only to disuse without denervation. 相似文献
6.
Traumatic peripheral nerve lesions characteristically result in denervation muscular atrophy. Atrophy of disuse may take place concomitantly, either proximal, adjacent to or distal to the denervation muscular atrophy. The degree of atrophy of disuse depends upon the severity of the nerve lesion. Clinically, it is difficult to determine where true denervation muscular atrophy ends and accompanying atrophy of disuse begins. In such circumstances a clinician may be misled into belief that the cause of so apparently extensive a lesion is elsewhere. The patient then is often submitted to other complex diagnostic procedures and treatments. This difficulty can usually be dissipated by the use of electromyography, for each specific type of muscular atrophy produces its own characteristic electromyographic changes. Disuse atrophy produces no changes in electrical activity, whereas denervation atrophy manifests itself by typical denervation activity. Moreover it is possible to determine what part of muscular atrophy in a given area is owing to damage to a nerve and what part is owing only to disuse without denervation. 相似文献
7.
Preena Nagpal Pamela J. Plant Judy Correa Alexandra Bain Michiko Takeda Hiroshi Kawabe Daniela Rotin James R. Bain Jane A. E. Batt 《PloS one》2012,7(10)
Skeletal muscle atrophy is a consequence of muscle inactivity resulting from denervation, unloading and immobility. It accompanies many chronic disease states and also occurs as a pathophysiologic consequence of normal aging. In all these conditions, ubiquitin-dependent proteolysis is a key regulator of the loss of muscle mass, and ubiquitin ligases confer specificity to this process by interacting with, and linking ubiquitin moieties to target substrates through protein∶protein interaction domains. Our previous work suggested that the ubiquitin-protein ligase Nedd4-1 is a potential mediator of skeletal muscle atrophy associated with inactivity (denervation, unloading and immobility). Here we generated a novel tool, the Nedd4-1 skeletal muscle-specific knockout mouse (myoCre;Nedd4-1flox/flox) and subjected it to a well validated model of denervation induced skeletal muscle atrophy. The absence of Nedd4-1 resulted in increased weights and cross-sectional area of type II fast twitch fibres of denervated gastrocnemius muscle compared with wild type littermates controls, at seven and fourteen days following tibial nerve transection. These effects are not mediated by the Nedd4-1 substrates MTMR4, FGFR1 and Notch-1. These results demonstrate that Nedd4-1 plays an important role in mediating denervation-induced skeletal muscle atrophy in vivo. 相似文献
8.
Regulation of Taurine Transport in Rat Skeletal Muscle 总被引:2,自引:1,他引:1
Taurine concentration of soleus muscle (SL, slow-twitch) was initially about twofold higher than that of extensor digitorum longus muscle (EDL, fast-twitch). Taurine concentration in gastrocnemius muscle (GC) was intermediate between that of EDL and SL. Four days after sciatic nerve section, taurine concentration in the EDL but not in the SL was increased by 2.5-fold. The increase was not due to the muscle atrophy and was observed 28 days after denervation. Tenotomy did not increase the total taurine content of the EDL. The increase in taurine concentration of the denervated EDL was prevented by simultaneous ingestion of guanidinoethane sulfonate, a competitive inhibitor of taurine transport. The initial and the maximal rates of [3H]taurine uptake were significantly higher in SL than in EDL. Denervation dramatically accelerated the initial and the maximal rates of the transport in EDL, whereas it significantly reduced those in SL. In contrast, the electrical stimulation of sciatic nerve accelerated the uptake of taurine by EDL and SL of the control but not of the curare-treated rats. These results suggest that transport of taurine into rat skeletal muscles is regulated differently by neural information and by muscular activity, and that the regulation is dependent on the muscle phenotype. 相似文献
9.
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. 相似文献
10.
Beehler BC Sleph PG Benmassaoud L Grover GJ 《Experimental biology and medicine (Maywood, N.J.)》2006,231(3):335-341
The ubiquitin-proteasome system is the primary proteolytic pathway implicated in skeletal muscle atrophy under catabolic conditions. Although several studies showed that proteasome inhibitors reduced proteolysis under catabolic conditions, few studies have demonstrated the ability of these inhibitors to preserve skeletal muscle mass and architecture in vivo. To explore this, we studied the effect of the proteasome inhibitor Velcade (also known as PS-341 and bortezomib) in denervated skeletal muscle in rats. Rats were given vehicle or Velcade (3 mg/kg po) daily for 7 days beginning immediately after induction of muscle atrophy by crushing the sciatic nerve. At the end of the study, the rats were euthanized and the soleus and extensor digitorum longus (EDL) muscles were harvested. In vehicle-treated rats, denervation caused a 33.5 +/- 2.8% and 16.2 +/- 2.7% decrease in the soleus and EDL muscle wet weights (% atrophy), respectively, compared to muscles from the contralateral (innervated) limb. Velcade significantly reduced denervation-induced atrophy to 17.1 +/- 3.3% in the soleus (P < 0.01), a 51.6% reduction in atrophy associated with denervation, with little effect on the EDL (9.8 +/- 3.2% atrophy). Histology showed a preservation of muscle mass and preservation of normal cellular architecture after Velcade treatment. Ubiquitin mRNA levels in denervated soleus muscle at the end of the study were significantly elevated 120 +/- 25% above sham control levels and were reduced to control levels by Velcade. In contrast, testosterone proprionate (3 mg/kg sc) did not alleviate denervation-induced skeletal muscle atrophy but did prevent castration-induced levator ani atrophy, while Velcade was without effect. These results show that proteasome inhibition attenuates denervation-induced muscle atrophy in vivo in soleus muscles. However, this mechanism may not be operative in all types of atrophy. 相似文献
11.
Neural Regulation of Muscle Glucose 6-Phosphate Dehydrogenase: Effect of Batrachotoxin and Tetrodotoxin 总被引:1,自引:1,他引:0
Stephen R. Max Sharad S. Deshpande Edson X. Albuquerque 《Journal of neurochemistry》1982,38(2):386-391
Abstract: We tested the hypothesis that glucose 6-phosphate dehydrogenase (G6PD) activity in the rat skeletal muscle is regulated by putative axonally derived neurotrophic factors. This was accomplished by comparing the effects of nerve section and subperineural injection of batrachotoxin (BTX) or tetrodotoxin (TTX) on G6PD in rat extensor digitorum longus (EDL) muscle. BTX, an agent known to block nerve impulse conduction and axonal transport, increased G6PD activity to 155% and 163% of control by days 2 and 4 after injection. Denervation of the EDL muscle by section of the peroneal nerve 10–20 mm from its entrance to the muscle caused G6PD activity to increase to 170% of control by day 1 and to 200% and 180% of control by days 2 and 4, respectively. The increase in enzyme activity after denervation and after subperineural injection of BTX was due in part to muscle inactivity resulting from blockade of nerve impulses. This conclusion is based upon the observation that subperineural injection of TTX at an identical site in the peroneal nerve caused a small but significant (30%) increase in G6PD activity after 4 days. Choline acetyltransferase (CAT) activity was assessed as a measure of the efficacy of blockade of slow axonal transport. Decreases in CAT activity following denervation or injection of BTX or TTX were parallel to increases in G6PD activity observed under these conditions. These results argue for a role of axonal transport in neural regulation of muscle G6PD, with a small contribution by neuromuscular activity. 相似文献
12.
The effect of reinnervation on the activities of prolyl 4-hydroxylase (PH) and galactosylhydroxylysyl glucosyltransferase (GGT), both enzymes of collagen biosynthesis, and on the concentration of hydroxyproline (Hyp) was studied in gastrocnemius, soleus, and tibialis anterior muscles of rat 19, 26, 40, and 61 days after crush denervation of the sciatic nerve. The GGT activity was elevated in denervated gastrocnemius and soleus muscles and the PH activity in gastrocnemius. Muscular Hyp concentration was increased in denervated tibialis anterior muscle. Both the PH and GGT activities and the Hyp concentration returned to the control level during the reinnervation period (19-61 days from the start of denervation). It seems that denervation atrophy of skeletal muscle is associated with an increased rate of muscular collagen biosynthesis and that during reinnervation collagen synthesis rate decreases despite accelerated muscular growth. The results thus suggest that innervation is a powerful suppressive regulator of muscular collagen biosynthesis. 相似文献
13.
Aydin MA Mackinnon SE Gu XM Kobayashi J Kuzon WM 《Plastic and reconstructive surgery》2004,113(6):1712-1718
Using a rat hindlimb model, the authors tested the hypothesis that, in muscles reinnervated after long-term denervation, atrophy-dependent and atrophy-independent mechanisms operate independently to produce force deficits. In adult rats, gastrocnemius muscles were subjected to denervation via tibial nerve transection. Reconstruction of the nerve lesion was delayed for periods ranging from 2 weeks to 1 year. After a minimum recovery period of 6 months after nerve repair, muscle mass and maximum isometric tetanic force were measured and specific force was calculated for each muscle (n = 40 muscles from 23 animals). After recovery, observed deficits in muscle mass and maximum tetanic force were directly proportional to the denervation interval. On the other hand, the deficit in specific force was not proportional to the denervation interval; all groups in which the nerve reconstruction was delayed for a month or longer demonstrated a deficit of 30 percent to 50 percent. These data support our hypothesis that, after prolonged denervation followed by reinnervation, the magnitude of the deficit in whole muscle force does not parallel the deficit in specific force. These data support the idea that mechanisms governing muscle atrophy are independent of those resulting in specific force deficits. 相似文献
14.
A Cangiano L Lutzemberger 《Bollettino della Società italiana di biologia sperimentale》1979,55(19):1950-1955
Degeneration of afferent nerve fibres was induced in rats in order to observe its effects on the properties of the extra-junctional membrane of soleus muscle fibres. In one approach, removal of dorsal root ganglia L4 and L5 was accomplished in preparations with intact or impulse-blocked (with tetrodotoxin containing cuffs around the sciatic nerve) efferent innervation. Spike resistance to tetrodotoxin developed in the inactive deafferented preparations earlier and to a greater extent than in control, that is only impulse-blocked, preparations. In another series of experiments, efferent denervation alone proved to be less effective than the association of efferent and afferent denervation. On the other hand, section of the afferent fibres central to the dorsal root ganglia was without effect. These results are consistent with the interpretation that products of nerve degeneration contribute together with inactivity to the development of the extrajunctional membrane changes observed in skeletal muscle after denervation. 相似文献
15.
This study was designed to determine whether the reductions in GLUT-4 seen in 3-day-denervated muscles can be prevented through chemical activation of 5'-AMP-activated protein kinase (AMPK). Muscle AMPK can be chemically activated in rats using subcutaneous injections with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). In this study, the tibial nerve was sectioned on one side; the other was sham operated but without nerve section. Acute injections of AICAR resulted in significantly increased AMPK activity in denervated gastrocnemius but not soleus muscles. Acetyl-CoA carboxylase activity, a reporter of AMPK activation, declined in both gastrocnemius and soleus in both denervated and contralateral muscles. Three days after denervation, GLUT-4 levels were significantly decreased by approximately 40% in gastrocnemius muscles and by approximately 30% in soleus muscles. When rats were injected with AICAR (1 mg/g body wt) for 3 days, the decline in GLUT-4 levels was prevented in denervated gastrocnemius muscles but not in denervated soleus muscles. The extent of denervation-induced muscle atrophy was similar in AICAR-treated vs. saline-treated rats. These studies provide evidence that some effects of denervation may be prevented by chemical activation of the appropriate signaling pathways. 相似文献
16.
D F Goldspink 《Comparative biochemistry and physiology. B, Comparative biochemistry》1978,61(1):37-41
1. Changes in protein turnover of the soleus and EDL muscles of adult mice have been studied 1, 7 and 80 days after denervation. 2. Increased rates of protein degradation 7 and 80 days post-denervation correlated with the atrophy and loss of protein from these muscles. 3. Rates of protein synthesis in the EDL decreased 24 hr after nerve section. However, these synthetic rates increased again to become higher in the 7 day denervated muscles compared with their controls. These latter anabolic changes are inconsistent with the concept of a denervated muscle being inactive. 4. These findings have been compared with a similar study on muscles of growing rats. Any passive stretching of the denervated muscles by continued bone growth appears unlikely to be a crucial factor explaining the increased rates of protein synthesis 7 days after denervation. 相似文献
17.
Junjian Jiang Ping Yao Yudong Gu Lei Xu Jianguang Xu Haitao Tan 《Cellular and molecular neurobiology》2012,32(8):1287-1298
To evaluate the function of rat mesenchymal stem cells (rMSCs) on denervated gastrocnemius muscles and to address the role of ciliary neurotrophic factor (CNTF) in rMSCs, denervated Wistar rats were separately injected with culture media (sham control), CNTF protein, 2.5?×?105 siCNTF-treated rMSCs, 2.5?×?105 GFP-transfected rMSCs, or 2.5?×?105 untreated rMSCs. Muscle function was assessed at different time points post-surgery. Tibial nerve and gastrocnemius muscle samples were taken at 4, 8, and 12?weeks for histochemistry, and neuromuscular junction repair was also examined by electron microscopy. Fluorescence immunocytochemistry on tissue sections confirmed neurotrophin expression in rMSCs but with little evidence of neuronal differentiation. The engraftment of rMSCs significantly preserved the function of denervated gastrocnemius muscle based both on evaluation of muscle function and direct examination of muscle tissue. Further, the density and depth of the junctional folds were visibly reduced 12?weeks after surgery and transplantation, especially in control group. Knockdown of CNTF expression in rMSCs failed to block muscle preservation, although administration of CNTF protein alone inhibited muscle atrophy, which indicating that delivery of rMSCs could preserve gastrocnemius muscle function following denervation and post-junctional mechanisms involved in the repairing capability of rMSCs. 相似文献
18.
Mohamed-Mounir El Mendili Timothée Lenglet Tanya Stojkovic Anthony Behin Raquel Guimar?es-Costa Fran?ois Salachas Vincent Meininger Gaelle Bruneteau Nadine Le Forestier Pascal Laforêt Stéphane Lehéricy Habib Benali Pierre-Fran?ois Pradat 《PloS one》2016,11(4)
PurposeThe mechanisms underlying the topography of motor deficits in spinal muscular atrophy (SMA) remain unknown. We investigated the profile of spinal cord atrophy (SCA) in SMN1-linked SMA, and its correlation with the topography of muscle weakness.ResultsCSA measurements revealed a significant cord atrophy gradient mainly located between C3 and C6 vertebral levels with a SCA rate ranging from 5.4% to 23% in SMA patients compared to controls. RD was significantly lower in SMA patients compared to controls in the anterior-posterior direction with a maximum along C4 and C5 vertebral levels (p-values < 10−5). There were no correlations between atrophy measurements, strength and disability scores.ConclusionsSpinal cord atrophy in adult SMN1-linked SMA predominates in the segments innervating the proximal muscles. Additional factors such as neuromuscular junction or intrinsic skeletal muscle defects may play a role in more complex mechanisms underlying weakness in these patients. 相似文献
19.
Chun-Jung Chen Fu-Chou Cheng Hong-Lin Su Meei-Ling Sheu Zong-Han Lu Chien-Yi Chiang Dar-Yu Yang Jason Sheehan Hung-Chuan Pan 《PloS one》2015,10(5)
PurposeThe skeletal muscle develops various degrees of atrophy and metabolic dysfunction following nerve injury. Neurotrophic factors are essential for muscle regeneration. Human amniotic fluid derived stem cells (AFS) have the potential to secrete various neurotrophic factors necessary for nerve regeneration. In the present study, we assess the outcome of neurological function by intramuscular injection of AFS in a muscle denervation and nerve anastomosis model.ResultsNT-3 (Neurotrophin 3), BDNF (Brain derived neurotrophic factor), CNTF (Ciliary neurotrophic factor), and GDNF (Glia cell line derived neurotrophic factor) were highly expressed in AFS cells and supernatant of culture medium. Intra-muscular injection of AFS exerted significant expression of several neurotrophic factors over the distal end of nerve and denervated muscle. AFS caused high expression of Bcl-2 in denervated muscle with a reciprocal decrease of Bad and Bax. AFS preserved the muscle morphology with high expression of desmin and acetylcholine receptors. Up to two months, AFS produced significant improvement in electrophysiological study and neurological functions such as SFI (sciatic nerve function index) and Catwalk gait analysis. There was also significant preservation of the number of anterior horn cells and increased nerve myelination as well as muscle morphology.ConclusionIntramuscular injection of AFS can protect muscle apoptosis and likely does so through the secretion of various neurotrophic factors. This protection furthermore improves the nerve regeneration in a long term nerve anastomosis model. 相似文献
20.
Mark A. Feger Jonathan Isaacs Satya Mallu Dorne Yager Mary Shall Gaurangkumar Patel Omar Protzuk Akhil S. Bokkisam 《Journal of brachial plexus and peripheral nerve injury》2022,17(1):e12
Background Muscle recovery following peripheral nerve repair is sup-optimal. Follistatin (FST), a potent muscle stimulant, enhances muscle size and satellite cell counts following reinnervation when administered as recombinant FST DNA via viral vectors. Local administration of recombinant FST protein, if effective, would be more clinically translatable but has yet to be investigated following muscle reinnervation. Objective The aim of this study is to assess the effect of direct delivery of recombinant FST protein on muscle recovery following muscle reinnervation. Materials and Methods In total, 72 Sprague-Dawley rats underwent temporary (3 or 6 months) denervation or sham denervation. After reinnervation, rats received FST protein (isoform FS-288) or sham treatment via a subcutaneous osmotic pump delivery system. Outcome measures included muscle force, muscle histomorphology, and FST protein quantification. Results Follistatin treatment resulted in smaller muscles after 3 months denervation ( p = 0.019) and reduced force after 3 months sham denervation ( p < 0.001). Conversely, after 6 months of denervation, FST treatment trended toward increased force output ( p = 0.066). Follistatin increased satellite cell counts after denervation ( p < 0.001) but reduced satellite cell counts after sham denervation ( p = 0.037). Conclusion Follistatin had mixed effects on muscle weight and force. Direct FST protein delivery enhanced satellite cell counts following reinnervation. The positive effect on the satellite cell population is intriguing and warrants further investigation. 相似文献