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PubMed1998

Effects of denervation and muscle inactivity on the organization of F-actin.

To discriminate between the influences of a motoneuron and muscle activity on the conformation of actin filaments, the extrinsic polarized fluorescence [of rhodamine-phalloidin and N-(iodoacetylamine)-1-naphthylamine-5-sulfonic acid attached to F-actin] was measured in "ghost" fibers from intact rat soleus muscles and atrophying muscles after denervation, immobilization, or tenotomy. The results show that the conformation of F-actin changed in all the atrophying muscles, but differently. In the denervated muscle, the flexibility of the actin filaments decreased, whereas in the other experimental muscles it remained as in the intact muscle. In the denervated muscle, the mobility of the C-terminus of the actin polypeptide increased. Attachment of myosin subfragment-1 influenced the F-actin conformation differently in the denervated muscle than in the other muscles studied. These results suggest that changes in the conformation of the actin filament are induced by the lack of connection with the motoneuron rather than by muscle inactivity.

Actins↗
PubMed1979

Effects of motor nerve anesthesia and tenotomy on muscle membrane properties.

Motor nerves to soleus muscles of rats were kept anesthetized for up to 7 days by applying solutions of lidocaine base or marcaine HCl. The anesthetic solutions were delivered from a subcutaneously located ALZA-minipump and reached the nerves through silastic cuffs. The ACh supersensitivity of muscles inactivated by nerve anesthesia for 3--7 days was comparable to that of muscles denervated for the same length of time. gm/gk (the ratio of total membrane conductance to the membrane K conductance) decreased from a normal value of 5--10 to less than two in 6--7 days, in anesthetic-inactivated and denervated muscles. The results were variable after 3 days of anesthesia. gm/gk of muscles which were tenotomized for 3 weeks was unchanged. The voltage-current curve for muscles kept in a solution containing 50 mM K propionate, which is steep at +50 mV, was less steep in denervated and anesthetic-inactivated, but not in tenotomized muscles, although atrophy was marked in all non-normal muscles.

Acetylcholine↗
PubMed1983

Experimental study of denervated rat muscle. Part II: The effects of electrical stimulation on the denervated rat muscles.

Electrical stimulation has been widely employed for the treatment of peripheral nerve lesion, however, its effects are not well known. Effects of electrical stimulation on denervated muscles were studied by measuring the weight of anterior crural muscles and the diameter of muscle fibers of the extensor digitorum longus muscle of the rat. The muscle fibers were classified by myofibrillar ATPase reaction. The denervated muscle showed loss of weight, a marked decrease in diameter of type 1 fibers and a small increase in diameter of type 2 fibers. Electrical stimulation suppressed weight loss of the denervated muscles. Electrical stimulation with high frequency cycle, like phasic motoneuron discharges, significantly suppressed the increase in diameter of type 2 muscle fibers. Electrical stimulation with low frequency cycle, like tonic motoneuron discharge, significantly suppressed the decrease in diameter of type 1 muscle fibers.

Adenosine Triphosphatases↗
PubMed1989

Dual effects of charged amphiphiles on depolarization-contraction coupling in denervated rat soleus muscle.

Ionic currents and contraction were recorded under voltage clamp conditions in single fibres isolated from rat soleus muscles denervated for more than 20 days. The effects of amphiphiles on depolarization-contraction (d.c.) coupling in Na-free TEA-containing solutions were analyzed. An anionic amphiphile, sodium dodecyl sulfate (1-10 microM), caused a dose-dependent reduction of the contractile response at all amplitudes of depolarization while a cationic amphiphile, dodecyltrimethylamine (1-10 microM), increased the maximum developed tension with a shift in the contractile threshold. A neutral amphiphile, lauryl acetate (20 microM), induced no significant variation. The effects of charged amphiphiles were found to be strongly dependent on the external calcium concentration and on membrane potential. The effect of sodium dodecyl sulfate to decrease tension was reduced or changed to positive inotropy following hyperpolarization of the membrane by, respectively, +10 and +20 mV. In hyperpolarized (+20 mV) cells, dodecyltrimethylamine reduced the amplitude of the contraction. The results demonstrated that changes in Ca-binding properties of surface membrane modified d.c. coupling in denervated slow twitch skeletal muscle.

Animals↗
PubMed1990

Acetylcholine-induced currents in denervated mouse soleus muscle: effects of antagonists.

Acetylcholine-induced currents were measured in partially depolarized mouse soleus muscles, denervated for 3-6 days by using a point voltage clamp. When 0.25 microM d-tubocurarine (d-Tc) was used, the weak currents provoked by 0.1 microM ACh, at a holding potential of -20 mV, were barely affected, while the large currents provoked by 2-5 microM ACh were decreased by more than 50%. By contrast, weak and strong ACh-induced currents were proportionally diminished when, under similar conditions, 20-100 microM ipratropium was used. Currents were proportionally diminished by d-Tc when the holding potential was set at +15 mV, a level corresponding to the reversal potential of the current provoked by small concentrations of ACh. In non-denervated flexor digitorum brevis muscles, d-Tc had the same relative effect at small and at large concentrations of ACh, independent of the holding potential. The reversal potential for the ACh-induced currents was about +14 mV for small concentrations of ACh and decreased to about +3 mV with 4 microM ACh in denervated soleus muscles. It was concluded that denervated soleus muscles, in contrast to the endplate regions of non-denervated mouse muscles, contain a small proportion of highly ACh-sensitive, weakly d-Tc-sensitive, predominantly Na(+)-permeable ACh receptors. These receptors are presumably responsible for the non-fading ACh-induced currents, described before, for the denervated mouse soleus muscle.

Acetylcholine↗
PubMed1988

Expression of actin mRNAs in denervated chicken skeletal muscle.

The expression of actin genes in chicken pectoralis muscle denervated 1 week after hatching was examined 1-8 weeks after the operation by RNA blot hybridization using a generic actin cDNA probe and DNA probes specific for alpha-skeletal and alpha-cardiac actin genes. Total and alpha-skeletal actin mRNAs/microgram total RNA decreased to about half of the levels found in contralateral control muscle, while the expression of alpha-cardiac actin mRNA was up-regulated. Consequently, alpha-cardiac actin mRNA formed about 15% of the total actin mRNA as compared to less than 1% found in control muscle. The expression of actin genes in the denervated muscle was similar to that in the late embryonic muscle. These results suggest that innervation is required to show the expression pattern of striated muscle actin genes found in mature muscle.

Actins↗
PubMed1972

Binding of -bungarotoxin to acetylcholine receptors in mammalian muscle (snake venom-denervated muscle-neonatal muscle-rat diaphragm-SDS-polyacrylamide gel electrophoresis).

Experiments were performed to determine the specificity of [(125)I]alpha-bungarotoxin binding to skeletal muscle. In adult rat diaphragm, [(125)I]alpha-bungarotoxin was found to bind almost exclusively to those regions of the muscle that contain endplates and are known to be sensitive to acetylcholine. In contrast, chronically denervated adult muscle and muscle from neonatal rats, both of which are sensitive along their entire lengths, bound substantial amounts of toxin in all regions. Toxin binding to all muscles was inhibited by d-tubocurarine and by carbamylcholine, but not by atropine. The bound [(125)I]toxin was solubilized by homogenization of the tissue in 1% Triton X-100 and was recovered as a single band, distinct from free toxin, after zone sedimentation. Treatment of the solubilized, toxin-bound complex with 2-mercaptoethanol and sodium dodecyl sulfate resulted in the recovery of free toxin. A toxin-bound complex was also obtained when toxin was incubated directly with extracts of muscle endplate regions prepared by homogenization in Triton X-100. No such complex was observed with extracts prepared from muscle lacking endplates. These results are consistent with the interpretation that alpha-bungarotoxin binds specifically to the acetylcholine receptor of mammalian skeletal muscle.

Acrylamides↗
PubMed2004

NGF, BDNF, NT-3, and GDNF mRNA expression in rat skeletal muscle following denervation and sensory protection.

Poor muscle and nerve functional recovery after nerve damage is a serious clinical problem, particularly if there is prolonged delay before nerve-muscle contact is reestablished. Our previous studies showed that sensory nerve cross-anastomosis (sensory protection) provides support to the denervated muscle. In the present study, we analyzed neurotrophic factor mRNA expression by RT-PCR in denervated rat gastrocnemius muscle receiving sensory protection with the saphenous nerve, compared to normal innervated muscle, to denervated muscle, and to denervated muscle repaired immediately with the peroneal (motor) nerve, after periods of 3 days to 3 months. No significant differences in mRNA levels of beta-actin, nerve growth factor, brain-derived neurotrophic factor or neurotrophin-3 were found between the sensory protection treatment and the denervated or the motor repair groups. However, sensory protection resulted in levels of muscle glial cell line-derived neurotrophic factor mRNA expression that were lower than in denervated muscle and higher than in muscle given immediate motor repair. These results demonstrate that glial cell line-derived neurotrophic factor mRNA is elevated following denervation but is partially down-regulated by sensory protection. Our study suggests that sensory protection provides a modified trophic environment by modulating neurotrophic factor synthesis in muscle.

Actins↗
PubMed1983

Experimental study of denervated rat muscle. Part I: Histochemical and electrophysiological observations of denervated rat muscle.

Histochemical and electrophysiological observations were carried out on denervated rat muscles, mainly extensor digitorum longus muscle. The myofibrillar ATPase reaction was employed to classify the type of muscle fibers. Type 1 fiber, low ATPase activity, and type 2 fiber, high ATPase activity, were recognized. It is generally believed that denervation causes a preferential atrophy of type 2 fibers and these fibers may be more dependant on neural influence than type 1 fibers. But the result of this investigation revealed that the atrophy of type 1 fiber and the enlargement of type 2 fiber will be caused by denervation. The term of enlargement is not equivalent to hypertrophy. Enlargement means the increasing of diameter of muscle fiber reacting to the denervation in this experiment. It is deduced that type 1 fiber is affected more by neural control than type 2 fiber.

Adenosine Triphosphatases↗
PubMed1985

Electrogenic Na-K pump in denervated mouse soleus muscles: prolonged activation by briefly applied acetylcholine.

Thin preparations of mouse soleus muscles denervated for 3-11 days were bathed in Cl-free solutions. The membrane potential (microelectrode technique) was an average of -65.6 mV. On application of 10 microM acetylcholine (ACh) the membrane potential fell to -2 to -8 mV. Following the washout of ACh it returned to values 9-24 mV more negative than before ACh. The membrane potential gradually returned toward the initial level during the ensuing 40-60 min. No hyperpolarization occurred when Na ions were absent during the application and washout of ACh or in the presence of 0.1 mM ouabain. The hyperpolarization was enhanced by replacing the Na ions by Li or Tris ions following an application of ACh in the presence of Na+. The hyperpolarization was suppressed by ouabain irrespective of whether the drug was applied in the presence or absence of Na+. The membrane potential was diminished by reducing [K+] from 4 to 1 mM in the absence of Na+ before ACh, but it was increased by the same procedure by up to 20 mV following the application of ACh. This indicates that the hyperpolarization was not entirely due to a K-depleting action of the Na-K pump at the membrane surface.

Acetylcholine↗
PubMed2004

Muscle-nerve-muscle neurotization for the reinnervation of denervated somatic muscle.

Muscle-Nerve-Muscle (MNM) is the reinnervation of a denervated (recipient) muscle via a nerve graft inserted into the belly of an innervated (donor) muscle. MNM is studied for the reinnervation of intrinsic denervated somatic skeletal muscle by evaluating both restored muscle contractile ability and innervation state. In a rat model, muscle function is tested following MNM neurotization from an innervated (donor), extensor digitorum longus muscle to a denervated (recipient), peroneus digit quinti (PDQ) muscle. PDQ muscle cross-sections labeled for neural cell adhesion molecule protein (NCAM), a marker for fiber denervation. MNM neurotization results in the recovery of PDQ muscle force generating capacity (58% of Normal-control) and a significantly lower percentage of residual muscle fiber denervation (38% denervated) compared with the Denervated-control (79% denervated) group. MNM neurotization reinnervates 62% of the previously denervated muscle fibers in the PDQ muscle. No decrement in force capacity is observed in the donor EDL muscle. Nerve grafting for MNM neurotization may restore modest contractile function to denervated muscle and reinnervate relatively more denervated muscle fibers than the Denervated-control.

Anatomy, Cross-Sectional↗
PubMed2006

A novel approach for screening the proteome for changes in protein conformation.

Changes in surface hydrophobicity are generally considered as a sensitive indicator for monitoring the structural alterations of proteins that are often associated with changes in function. Currently, no technique has been developed to screen a complex mixture of proteins for changes in the conformation of specific proteins. In this study, we adapted a UV photolabeling approach, using an apolar fluorescent probe, 4,4'-dianilino-1,1'-binaphthyl-5,5'-disulfonic acid (BisANS), to monitor changes in surface hydrophobic domains in either purified rhodanese or skeletal muscle cytosolic proteins by urea-induced unfolding or in response to in vitro metal-catalyzed oxidation. Using two-dimensional polyacrylamide gel electrophoresis (2D PAGE), we identified two specific proteins in skeletal muscle cytosol that exhibited a marked loss of incorporation of BisANS after exposure to in vitro oxidative stress: creatine kinase (CK) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). We found that the activities of both enzymes were also reduced significantly in response to oxidative stress. We then determined if this method could detect changes in surface hydrophobicity in specific proteins arising from oxidative stress generated in vivo by muscle denervation. A loss in surface hydrophobic domains in CK and GAPDH was again observed as measured by the BisANS photoincorporation approach. In addition, the CK and GAPDH activity in denervated muscle was markedly reduced. These data demonstrate for the first time that this assay can screen a complex mixture of proteins for alterations in surface hydrophobic domains of individual proteins.

Animals↗
PubMed1978

Effects of disuse and nerve stump length on the development of fibrillation in denervated soleus muscle.

Both in normal (control) and in cordotomized (disused) rats, the soleus muscle was denervated either by cutting the sciatic nerve near the trochanter (proximal denervation) or by cutting the soleus nerve near the insertion into the muscle (distal denervation). In the control muscles, the development of fibrillation was not dependent on the level of nerve section. In disused muscles, the development of fibrillation was greater following distal denervation that following the proximal one.

Animals↗
PubMed1986

Molecular forms of N-CAM and its RNA in developing and denervated skeletal muscle.

The neural cell adhesion molecule (N-CAM) is present in both embryonic and perinatal muscle, but its distribution changes as myoblasts form myotubes and axons establish synapses (Covault, J., and J. R. Sanes, 1986, J. Cell Biol., 102:716-730). Levels of N-CAM decline postnatally but increase when adult muscle is denervated or paralyzed (Covault, J., and J. R. Sanes, 1985, Proc. Natl. Acad. Sci. USA., 82:4544-4548). To determine the molecular forms of N-CAM and N-CAM-related RNA during these different periods we used immunoblotting and nucleic acid hybridization techniques to analyze N-CAM and its RNA in developing, cultured, adult, and denervated adult muscle. As muscles develop, the extent of sialylation of muscle N-CAM decreases, and a 140-kD desialo form of N-CAM (generated by neuraminidase treatment) is replaced by a 125-kD form. This change in the apparent molecular weight of desialo N-CAM is paralleled by a change in N-CAM RNA: early embryonic muscles express a 6.7-kb RNA species which hybridizes with N-CAM cDNA, whereas in neonatal muscle this form is largely replaced by 5.2- and 2.9-kb species. Similar transitions in the desialo form of N-CAM, but not in extent of sialylation, accompany differentiation in primary cultures of embryonic muscle and in cultures of the clonal muscle cell lines C2 and BC3H-1. Both in vivo and in vitro, a 140-kD desialo form of N-CAM and a 6.7-kb N-CAM RNA are apparently associated with myoblasts, whereas a 125-kD desialo form and 5.2- and 2.9-kb RNAs are associated with myotubes and myofibers. After denervation of adult muscle, a approximately 12-15-fold increase in the levels of N-CAM is accompanied by a approximately 30-50-fold increase in N-CAM RNA, suggesting that N-CAM expression is regulated at a pretranslational level. Forms of N-CAM and its RNA in denervated muscle are similar to those seen in perinatal myofibers.

Animals↗