SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Mitochondrial preparations derived from denervated rat skeletal muscle and paired control muscle are characterized with respect to their oxidative and phosphorylative capacities. Our data indicate that there is an impairment within the first 2 energy coupling regions of the respiratory chain and within the ATPase complex itself.
A striking correlation between insulin-like growth factor II (IGF-II) gene expression and turnover of neuromuscular synapses was observed. The IGF-II gene was expressed at a high level in fetal rat hind limb muscles prior to the developmental formation of synapses and increased while polyneuronal innervation accumulated. Thereafter, there was a selective down-regulation of IGF-II mRNAs that was exactly coincident with the postnatal time course for elimination of superfluous synapses. The hypothesis that innervation might provide a signal suppressing IGF-II gene expression was tested. Upon transection of the sciatic nerve, there was up-regulation of IGF-II mRNA content in muscle. This up-regulation was selective and correlated with the capacity of denervated muscle to accept reinnervation. These results suggest that the IGF-II gene may play a role in the development and turnover of synapses.
Motor neurons regulate the acetylcholine sensitivity of the muscles they innervate: denervated muscle fiber become "supersensitive" to acetylcholine, due to insertion of newly synthesized acetylcholine receptors (AChRs) in the plasma membrane. We used hybridization analysis with a cloned cDNA specific for AChR alpha-subunit to compare the abundance of AChR mRNA in innervated and denervated adult mouse muscles. Within 3 d of denervation, levels of AChR mRNA increased 100-fold; levels of actin mRNA changed little. The increase in AChR mRNA level was sufficiently large and rapid to account for denervation supersensitivity.
Explore the source record for details and available documents.
We have shown an increase of apamin receptors in rat skeletal muscle membranes following the application of colchicine to the sciatic nerve. 125I-apamin binding to partially purified membrane fractions was observed since day 4, reached a maximum around days 6-15, and was negligible at day 35 after the application of colchicine. Control muscles (nerves treated with buffer solution) showed low binding values (11 fmol/mg protein). Maximal 125I-apamin binding values to partially purified muscle membranes of colchicine-treated rats (42 fmol/mg protein) were lower than those obtained in denervated muscle (95 fmol/mg protein). The affinity binding constant values were 37 (colchicine) and 95 pM (denervation). No signs of muscle denervation were observed on histological examination of the nerve submitted to colchicine treatment nor in the muscles innervated by it. Muscle tension developed by indirect stimulation was the same as in controls. We here show also that partially purified membranes of normal untreated muscles have measurable amounts of 125I-apamin binding (13 fmol/mg protein), similar to those obtained in control muscles. Electromyographic recordings of the muscles after colchicine treatment of the nerve showed abnormal repetitive electrical discharges, similar to myotonic discharges, that were present with a similar temporal course as the increase in apamin receptors. The myotonic-like discharges were suppressed by the topical application of apamin to the muscle, whereas the toxin had no effect on anthracene-9-carbolytic acid-induced myotonia. Our results suggest that a neurotrophic factor that travels by axonal flow is involved in the regulation of the expression of apamin receptors in skeletal muscle membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
The resting membrane potential (RMP) of denervated muscle fibres of rat diaphragm muscle is depolarized by approximately 8-10 mV during the first 3 h after nerve section and this early postdenervation depolarization is reduced substantially by the presence of 5x10(-8) M acetylcholine (ACh) or carbachol (CB). The muscarinic antagonist atropine (Atr; 5x10(-9) to 5x10(-6) M) reduced the effect of CB in a dose-dependent manner (K(i)=7x10(-8) M) and increased the rate of the early postdenervation depolarization. In lower doses (5x10(-7) M), Atr acted only in the presence of an allosteric stabilizator hexamethylene-bis-[dimethyl-(3-phtalimidopropyl)ammonium] (W-84). Also pirenzepine, a specific inhibitor of the M1 subtype of muscarinic receptor, blocked the action of CB in a dose-dependent manner with an apparent inhibition constant K(i)=1x10(-7) microM. DAMP, a specific M3 antagonist, was without effect on the muscle hyperpolarization induced by CB. CB also hyperpolarized the membrane potentials of muscles which were denervated for 1-3 days. It is concluded that ACh and CB protect the muscle fibres from early depolarization through M1-cholinergic receptors on the muscle membrane. These particular receptors can apparently mediate the 'trophic', non-impulse regulation of RMP in skeletal muscles when they are activated by acetylcholine released non-quantally.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Muscle regeneration is a potentially useful model for defining the mechanisms responsible for nerve-dependent myosin isogene regulation in skeletal muscle. As a first step towards this goal we have characterized the pattern of expression of the four myosin heavy chain (MHC) genes, MHC-beta/slow, -2A, -2X and -2B isogenes, during early stages of muscle regeneration both in the presence and in the absence of the nerve. Muscle degeneration/regeneration was induced by intramuscular injection of the myotoxic drug, bupivacaine, in the rat slow soleus muscle. MHC transcripts were identified by in situ hybridization with specific riboprobes during the period from day 3 to day 7 after muscle injury. The four genes are not detected at day 3, when the regenerating muscle contains predominantly embryonic and neonatal MHC isoforms. MHC-2X and -2B transcripts are first detected at day 4 in both innervated and denervated muscles. These transcripts remain as major transcripts in denervated muscle whereas they are down-regulated by day 5 and disappear by day 6-7 in the presence of the nerve. Innervation induces strong up-regulation of MHC-2A at day 4 and MHC-beta/slow transcripts at day 5. MHC-2A transcripts are first homogeneously expressed in most fibers then become segregated in a minor population of fibers by day 6-7 while MHC-beta/slow transcripts increase in most fibers. In the absence of the nerve MHC-beta/slow transcripts are never expressed and MHC-2A transcripts are detected in rare fibers at days 5-7.
Explore the source record for details and available documents.
Muscle fibres of the rat diaphragm kept in a tissue culture medium became depolarized by 8-10 mV within 3 h after denervation. In the presence of carbachol (CB; 5 x 10(-8) M), and acetylcholine (ACh; 5 x 10(-8) M, the post-denervation depolarization was reduced. Both drugs were used in concentrations which mimicked the effect of non-quantal release of ACh. (+)Tubocurarine (TC) and ouabain did not prevent the protective action of CB, indicating that this effect is not mediated through ACh nicotinic receptors or the electrogenic Na+, K+ pump. Addition of Mg2+, verapamil, diltiazem, nifedipine and Cd2+ in concentrations which block Ca2+ entry virtually inhibited the effect of both cholinomimetics. L-Nitroarginine methylester (NAME), an inhibitor of NO synthase, and haemoglobin, an extracellular scavenger of the NO radical, completely eliminated the protective effect of CB on post-denervation depolarization. The retrograde action of NO produced by cholinomimetics on nerve terminals is postulated.
Explore the source record for details and available documents.
The purpose of this study is to observe changes in muscle after severance of its main innervation, especially the changes in its volume and weight. In ten rabbits, it was found that the reduction of the volume of gastrocnemius muscle flap was 47.8%, and that of gastrocnemius and soleus muscles was 50.5% one month after the severance of the tibial nerve, while their weights were decreased 47.6%, 51.3% and 46.9% respectively. After three months the respective reduction in volume was 40.3%, 32.3% and 38.8%, while the weight was reduced to 44.0%, 34.0 and 40.3%, respectively. Histological examination revealed capillary dilatation and congestion, decrease myofibrils and increase of adipose tissue. Evidence of diminution of muscular metabolism and energy consumption was found by histochemical study, including ATPase, phosphorylase, and succinic dehydrogenase staining. The result of electromyogram examination confirms the presence of muscle denervation.
The rapid development of hyperkalemia leading to cardiac arrest can occur in patients with spinal cord injuries and other conditions when succinylcholine is used during the induction of anesthesia. Three patients with thoracolumbar spinal cord injuries resulting in lower motor neuron lesions or lesions above the lower extremity motor units developed hyperkalemia followed by cardiac arrest after succinylcholine administration. The mechanism by which succinylcholine leads to hyperkalemia from denervated muscle is described and precautions to be taken are mentioned. Physicians caring for patients with denervated muscle due to spinal cord injuries should be aware of this danger and nondepolarizing muscle relaxants should be used instead of succinylcholine.
The sensitivity of the tongue muscles to acetylcholine was examined in repeated experiments on cats anaesthetized with hexobarbitone. The supersensitivity which developed after section of the hypoglossal nerve was found to decrease when the muscles, after cross-suture, became re-innervated from the vagus or the chorda-lingual nerve. The supersensitivity caused by denervation could also be reduced by injecting acetylcholine repeatedly during six hours in acute experiments.
Experimental material obtained on mouse extensor digitorum longus was presented concerning the dynamics of changes in the membrane potential (MP) of muscle fibres after chronic denervation (1-12 days), the effect of ouabain and increase of extracellular potassium on MP of normal and denervated muscles, changes of input resistance and volumes of muscle fibres after denervation.
OBJECTIVE: This investigation utilizes a single muscle fiber simulation to compare and contrast single muscle fiber waveform configurations arising from innervated and denervated tissue taking into account possible tissue-electrode interactions. METHODS: Intracellular action potentials (IAPs) from innervated and denervated muscle tissue are simulated. The extracellular waveform configurations as recorded from the fiber's midpoint (endplate in innervated tissue), halfway between the midpoint and fiber termination, as well as fiber termination for both innervated and denervated single muscle fibers are examined. Further, two types of muscle fiber terminations are assessed: (1) sealed end effect; and (2) compressed end effect. RESULTS: Irrespective of different types of IAPs, recordings from the fibers' middle, halfway between the midpoint and termination, as well as from the sealed end, revealed similar configurations. However, for the innervated fiber's compressed termination, a monophasic positive waveform was derived while the denervated fiber's compressed termination generated a prototypical positive sharp wave. CONCLUSIONS: It is hypothesized that the needle electrode can no longer be considered a passive recording device but may interact with the fiber so as to generate a sealed end or compressed end effect. Depending upon the type of needle-fiber interaction and the electrode's location with respect to the IAP's generation site, a limited number of potentials with specific configurations will be recorded for both innervated and denervated tissue. Further, depending upon the type of needle-tissue interaction, innervated muscle fibers can generate non-volitional waveforms with configurations similar to those recorded from denervated tissue. It is no longer sufficient to merely consider waveform configuration when attempting to define positive sharp waves and fibrillation potentials, but it is important now also to consider firing rate and rhythm.