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PubMed1976

Are muscle fibers denervated in myotonic dystrophy?

An underlying neurogenic abnormality has recently been postulated in the muscular dystrophies. To test this hypothesis, we applied a widely accepted criterion of denervation-ie, and increase in extrajunctional acetyicholine (ACh) receptor sites--to muscles biopsy specimens from nine patients with myotonic dystrophy and three with amyotrophic lateral scierosis (ALS). The ACh receptor sites were determined by means of iodine 125-labeled alpha-bungarotoxin binding, measured by scintillation counting and autoradiography. None of the myotonic dystrophy muscles showed increased extrajunctiona ACh receptor sites, even in the smallest fibers. By contrast, muscle biopsy specimens from patients with ALS showed notably increased extrajunctional ACh receptor sites, especially in the small fibers. Our findings do not support the hypothesis of a neurogenic defect in myotonic dystrophy.

Adult↗
PubMed1981

The uptake of 99mtechnetium diphosphonate into degenerating and regenerating muscle. A correlative histological and biochemical study.

The uptake of 99mTc-methylene diphosphonate into rat skeletal muscle has been studied. Uptake did not occur in normal or denervated muscles. Muscles damaged by exposure to the myotoxin notexin did accumulate label. The toxin causes a severe inflammatory, necrotising myopathy and regeneration normally begins 2-3 days after toxin administration. The uptake of label was maximal at 12-24 h, at which time muscle wet weight and cellular infiltration were also maximal. Label was found in the muscle mitochondria, the invading inflammatory cells and the oedema fluid. Regenerating muscles did not accumulate label. The uptake of label was positively correlated with total muscle calcium up to 24 h after the onset of necrosis, but it was suggested that the changes in the two parameters are not causally related.

Animals↗
PubMed1983

Exercise therapies in peripheral neuropathies.

The treatment of peripheral neuropathies should be aimed at maintaining the range of motion of the joints, re-educating the patient in skilled activities and optimizing the recovery of strength. Many techniques have been described to substitute for, to strengthen and to improve the function of residual innervated muscle; however, not all of these techniques are of unquestioned value. Specifically, electrical stimulation does not appear to enhance reinnervation of totally denervated muscle. Similarly, overstretching weakened muscle may impair the use of paretic muscle. Because overwork may damage partially denervated muscle, brief isometric or isotonic contractions may be more beneficial for increasing strength than a program of habitual exhausting activities.

Cold Temperature↗
PubMed1990

A quantitative assessment of extraocular muscle growth in peripheral nerve autografts.

In previous studies, we have documented new growth of extraocular muscle fibers within axon-depleted motor neurons of denervated muscle. This study was designed to quantitate the regenerative growth of extraocular muscle within autologous peripheral sensory nerve transplants and to determine whether acutely denervated extraocular muscle affects this growth. Fifteen anesthetized beagles were subjected to an intracranial lesion of the left third cranial nerve. Segments of the infraorbital sensory nerve were removed from the nose and implanted between the lateral rectus and inferior oblique muscles in both orbits. At 2, 4 and 8 weeks postoperatively, five dogs were killed and the nerve grafts were removed. Muscle fibers were counted at four levels along each nerve segment. Fiber number increased significantly at each successive postoperative interval in implanted nerve segments on both the denervated and nondenervated side. At 8 weeks, fiber number was significantly greater on the denervated side. These results indicate that autologous peripheral sensory nerve is capable of supporting regenerative growth of extraocular muscle and that denervation has a significant positive influence on muscle fiber growth.

Animals↗
PubMed2003

Smooth muscle cholinergic denervation hypersensitivity in diverticular disease.

BACKGROUND: Evidence from clinical and laboratory investigations into the causes of diverticular disease suggests that disturbances in cholinergic activity are important, the effector mechanisms of which have yet to be established. We aimed to investigate the role of smooth muscle and neural cholinergic activity in the pathogenesis of this disease. METHODS: Two investigators independently did a blinded immunohistochemical image analysis of localising antibodies to choline acetyltransferase, co-localised with protein gene product (PGP)--a marker of general neural tissue-and smooth muscle muscarinic M3 receptors, on three histological sections of sigmoid colons from ten patients with diverticular disease and ten controls, after resections for rectal tumours. We also did isotonic organ bath experiments to assess muscle strip sensitivities to exogenous acetylcholine. FINDINGS: In circular muscle, activity of choline acetyltransferase was lower in patients with diverticular disease than in controls: median percentage surface area of choline acetyltransferase over PGP was 17.5% (range 10.0-37.0) in patients with diverticular disease and 47.0% (29.0-54.0) in controls (p<0.0001). M3 receptors were upregulated in patients with diverticular disease compared with controls: the median surface area was 13.2% (6.0-23.3) in patients with diverticular disease and 2.5% (1.6-3.7) in controls (p<0.0001). The sensitivity to exogenous acetylcholine was increased in patients with diverticular disease (mean -log EC(50) 5.6 [SD 0.3]) compared with controls (4.9 [0.5]; difference 0.7 [95% CI 0.3-1.1], p=0.006). In longitudinal muscle, choline acetyltransferase activity was lower in patients with diverticular disease (median 19.5%, range 12.0-30.0) than in controls (47.0%, 35.0-60.0; p<0.0001), with upregulation of M3 receptors in diverticular disease (diverticular disease 7.8% [1.9-20.4], controls 1.7% [0.8-3.0]; p<0.0001). However, sensitivity to exogenous acetylcholine did not differ between the two groups (diverticular disease mean 5.6% [SD 0.3], controls 5.2% [0.4]; difference 0.4% [95% CI -0.02-0.7], p=0.06). INTERPRETATION: Our results suggest that cholinergic denervation hypersensitivity can affect smooth muscle. Upregulation of smooth muscle M3 receptors might account for specific clinical, physiological, and pharmacological abnormalities associated with diverticular disease.

Acetylcholine↗
PubMed2005

Muscle hypertrophy with complex repetitive discharges in C-6 radiculopathy.

OBJECTIVE: To report on a case of post-denervation muscle hypertrophy in an unusual distribution. CASE REPORT: A 52-year-old patient with severe flaccid paraparesis after polio developed unilateral C-6 radiculopathy that resolved with conservative treatment. Within 2 years marked hypertrophy, stiffness and pain in the muscles in the affected myotome developed. EMG discovered abundant complex repetitive discharges (CRD) within hypertrophic muscles. On biopsy, true hypertrophy of muscle fibers and some group atrophy was found. Steroid treatment relieved the symptoms and significantly suppressed the CRD. The possible causative role of CRD for hypertrophy in partially denervated muscle is discussed.

Humans↗
PubMed1986

Function dependent changes in the subcellular distribution of high energy phosphates in fast and slow rat skeletal muscles.

Function dependent changes in the subcellular distribution of ATP, ADP, creatine phosphate (CrP) and creatine (Cr) in rat fast-twitch gastrocnemius and slow-twitch soleus muscles were studied by fractionation of freeze-clamped and freeze-dried tissue in non-aqueous solvents. During 5 min of isotonic contraction of gastrocnemius muscles the mitochondrial content of total creatine [sigma(CrP + Cr)] decreases by 9.5 nmol/mg total protein whereas there is an increase in extramitochondrial total creatine by 12.3 nmol/mg total protein, indicating a net transfer of approximately 10 nmol total creatine/mg total protein/5 min across the mitochondrial inner membrane. During short-term stimulation (6 s) of gastrocnemius muscles the socalled "additionally-bound ADP" correlates not only with force (Hebisch et al. 1984) but also with filament overlap. This confirms the previous suggestion that "additionally-bound ADP" represents actomyosin-ADP-complexes. Following long-term stimulation (10 s), the rate of decay of force is at least two orders of magnitude faster than that of "additionally bound ADP". This indicates a decrease of actomyosin-ADP complexes due to formation of myosin-ADP complexes. Short-term stimulation (6 s) of slow-twitch soleus muscles does not lead to any force-dependent change in the content of "additionally-bound ADP", similar to the finding in long-term contracting gastrocnemius muscles. Denervation of soleus muscles leads to a decrease in "additionally-bound ADP" to values comparable to those found in resting fast-twitch gastrocnemius muscles.

Adenosine Diphosphate↗
PubMed2003

Electrodiagnosis of the anorectum: a review of techniques and clinical applications.

Electrodiagnostic tests may be valuable in the assessment of patients with anorectal dysfunction and are complementary to imaging and manometry. While the latter delineate morphological and functional sphincter changes, respectively, electrodiagnostic methods document, help to localize and assess the severity and mechanism of neural injury. These data are important for the treatment of patients and for estimating their prognoses. Among electrodiagnostic tests, concentric needle electromyography of the external anal sphincter is the most important. It demonstrates muscle denervation, quantitatively estimates muscle reinnervation, estimates the level of motor neuron excitability and assesses several kinesiological parameters. In addition, measurement of the bulbocavernosus reflex is often useful, while pudendal somatosensory evoked potentials are sometimes useful. Use of single tests of sacral nervous system by workers less familiar with theoretical principles of clinical neurophysiology is discouraged. In patients with suspected neurogenic bowel disorders, comprehensive electrodiagnostic approach, performed by clinical neurophysiologists experienced in application of these tests to the sacral nervous system, should complement data obtained by other methods and guide patient management.

Anus Diseases↗
PubMed1995

The hyper-reinnervation of rat skeletal muscle.

This study examines muscle recovery and related changes in the motor unit population of 'hyper-reinnervated' rat skeletal muscle. Medial gastrocnemius (MG) muscles were hyper-reinnervated by either cutting the MG nerve and implanting it on the MG muscle together with additional hind limb nerves, or by crushing the MG nerve and excising the medial portion (50-70%) of the MG muscle. Our findings were that muscles hyper-reinnervated with multiple nerves recovered muscle mass and strength more fully than did the self-reinnervated muscles, more motor units were formed (up to three times the normal number were found), and the mean motor unit size was significantly smaller. A relatively small percentage of muscle fibers became polyneuronally innervated. In contrast, the number of motor units that were formed in the muscle reduction experiments were not significantly larger than was expected considering the mass of the muscles. We conclude that hyper-reinnervation improves muscle recovery, it may be a useful technique for improving function in denervated muscle, and may serve to provide added sources of EMG control signals in some amputees.

Amputees↗
PubMed1995

Acetylcholine contractures of skeletal muscles: inhibition by chlorpromazine and diltiazem.

The maximum contractures evoked by 100 microM ACh of mouse soleus muscles denervated for 3-7 days are completely inhibited by a 10 min exposure to 100 microM chlorpromazine (CP). Recovery on washout of CP takes more than 1 hr to complete. ACh evoked contractures are also inhibited by diltiazem (D); washout of D is immediately followed by recovery. Electrically evoked twitches and K evoked contractures are largely unaffected by CP, caffeine evoked contractures are decreased but not abolished. Fast mouse and (non-denervated) frog tonic muscles behave similarly. Depolarization by ACh and ACh-evoked whole cell currents show enhanced desensitization at low, and block at high [CP] and [D]; more than 50% recovery is achieved by less than 1 min washout of CP and D. Currents carried by Na+ and Mg2+ ions behave similarly. It is concluded that activation of ACh evoked contractures may be blocked by CP independent of ionic currents through nicotinic ACh receptors and that it depends on intracellular processes linked to these receptors.

Acetylcholine↗
PubMed1986

Motoneurone survival factor produced by muscle increases in parallel with messenger RNA sequences homologous to beta NGF-cDNA.

Motoneurone survival in culture is enhanced by growth factors present in embryonic rat muscles and denervated adult muscles: extracts from mature muscle and 2-day denervated mature muscle do not produce survival effects whereas extracts from embryonic muscle and 4-day denervated mature muscle produce maximum survival effects. Here we show, using dot hybridization of mRNA with a 32P-labelled cDNA probe for beta-nerve growth factor (beta NGF), that mRNA sequences homologous to beta NGF appear in muscle in parallel with increased motoneurone survival activity. RNA gel blot hybridizations show that embryonic mRNA contains a sequence in the same molecular weight range as the mRNA for beta NGF.

Animals↗
PubMed2003

Glutamate regulation of non-quantal release of acetylcholine in the rat neuromuscular junction.

Glutamate, previously demonstrated to participate in regulation of the resting membrane potential in skeletal muscles, also regulates non-quantal acetylcholine (ACh) secretion from rat motor nerve endings. Non-quantal ACh secretion was estimated by the amplitude of endplate hyperpolarization (H-effect) following blockade of skeletal muscle post-synaptic nicotinic receptors by (+)-tubocurarine and cholinesterase by armin (diethoxy-p-nitrophenyl phosphate). Glutamate was shown to inhibit non-quantal release but not spontaneous and evoked quantal secretion of ACh. Glutamate-induced decrease of the H-effect was enhanced by glycine. Glycine alone also lowered the H-effect, probably due to potentiation of the effect of endogenous glutamate present in the synaptic cleft. Inhibition of N-methyl-d-aspartate (NMDA) receptors with (+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine (MK801), dl-2-amino-5-phosphopentanoic acid (AP5) and 7-chlorokynurenic acid or the elimination of Ca2+ from the bathing solution prevented the glutamate-induced decrease of the H-effect with or without glycine. Inhibition of muscle nitric oxide synthase by NG-nitro-l-arginine methyl ester (l-NAME), soluble guanylyl cyclase by 1H[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and binding and inactivation of extracellular nitric oxide (NO) by haemoglobin removed the action of glutamate and glycine on the H-effect. The results suggest that glutamate, acting on post-synaptic NMDA receptors to induce sarcoplasmic synthesis and release of NO, selectively inhibits non-quantal secretion of ACh from motor nerve terminals. Non-quantal ACh is known to modulate the resting membrane potential of muscle membrane via control of activity of chloride transport and a decrease in secretion of non-quantal transmitter following muscle denervation triggers the early post-denervation depolarization of muscle fibres.

Acetylcholine↗