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PubMed2006

Denervation alters mRNA levels of repair-associated genes in a rabbit medial collateral ligament injury model.

Previous experiments revealed that denervation impairs healing of the MCL. This suggested the hypothesis that denervation would decrease repair-associated mRNA levels in the injured MCL when compared with normally innervated injured MCL. Adult, skeletally mature female rabbits were assigned to one of four groups: unoperated control, femoral nerve transection alone (denervated controls), MCL partial tear or denervated MCL partial tear. At three days, two weeks, six weeks or sixteen weeks post-surgery, cohorts of 6 rabbits from each experimental group were killed. Ligaments were harvested, RNA extracted and RT-PCR was performed using rabbitspecific primers. In the denervated injury group, mRNA levels for the angiogenesis-associated gene MMP-13, matrix components Collagen I and III, growth factor TGF-beta and angiogenesis inhibitors TIMP-3, and TSP-1 had all increased by two-weeks post-injury, in comparison to the non-denervated injury group (p < or = 0.01). An increased level of TSP-1 mRNA was also detected in the denervated injured group at sixteen weeks post injury (p < or = 0.01). Contrary to the initial hypothesis, denervation led to increased mRNA levels for many relevant molecules during the early stages of MCL healing. Thus, inappropriate timing of over-expression of some molecules may potentially contribute to the decreased quality of the scar tissue, particularly molecules such as TSP-1. Neuronal derived factors strongly influence the in vivo metabolic activity of ligament and scar fibroblasts in the initial phases of healing.

Animals↗
PubMed2007

Electrical stimulation based on chronaxie reduces atrogin-1 and myoD gene expressions in denervated rat muscle.

Denervation induces muscle fiber atrophy and changes in the gene expression rates of skeletal muscle. Electrical stimulation (ES) is a procedure generally used to treat denervated muscles in humans. This study evaluated the effect of ES based on chronaxie and rheobase on the expression of the myoD and atrogin-1 genes in denervated tibialis anterior (TA) muscle of Wistar rats. Five groups were examined: (1) denervated (D); (2) D+ES; (3) sham denervation; (4) normal (N); and (5) N+ES. Twenty muscle contractions were stimulated every 48 h using surface electrodes. After 28 days, ES significantly decreased the expression of myoD and atrogin-1 in D+ES compared to the D group. However, ES did not prevent muscle-fiber atrophy after denervation. Thus, ES based on chronaxie values and applied to denervated muscles using surface electrodes, as normally used in human rehabilitation, was able to reduce the myoD and atrogin-1 gene expressions, which are related to muscular growth and atrophy, respectively. The results of this study provide new information for the treatment of denervated skeletal muscle using surface ES.

Animals↗
PubMed1982

Electrical stimulation of denervated muscle prevents decreases in oxidative enzymes.

The influence of muscular contraction on the oxidative enzymes and the diameters of muscle fibers was investigated. Soleus muscles of guinea pigs were denervated for four weeks. The denervated fibers showed a reduction in the intensity of staining for beta-hydroxybutyrate dehydrogenase, cytochrome oxidase, succinate dehydrogenase, and NADH-dependent tetrazolium reductase. Denervation also resulted in a decrease in fiber diameter. Denervated soleus muscles were electrically stimulated to contract over a four-week period at a frequency normally received by slow contracting muscles. Electrical stimulation caused the stain intensity of histochemical reactions for oxidative enzymes to appear to be normal or greater than normal in 90% of the denervated fibers. Stimulation also caused 69% of the denervated fibers to be of normal or greater than normal size. The results demonstrate that contraction of denervated muscle by electrical stimulation prevents the loss of oxidative enzymes and the atrophy associated with denervation.

Adenosine Triphosphatases↗
PubMed1990

Insulin effects in denervated and non-weight-bearing rat soleus muscle.

Previous reports indicated that glucose uptake in denervated muscle is resistant to insulin, while in non-weight-bearing (unweighted) muscle this effect of insulin is enhanced. To extend the comparison of these differences, insulin effects on amino acid uptake and protein metabolism were studied in soleus muscles subjected to denervation or unweighting. Denervated muscle showed insulin resistance of both 2-deoxy[1,2-3H]glucose and alpha-[methyl-3H]aminoisobutyric acid uptake whereas unweighted muscle showed an increased or normal response, respectively. Atrophy was greater in denervated than in unweighted muscle, apparently due to faster protein degradation. The stimulation of protein synthesis and the inhibition of protein degradation by insulin was generally less in denervated than in unweighted muscle. Since metabolic measurements in denervated-unweighted muscles did not differ from those in denervated-weight-bearing muscles, effects of denervation must be independent of leg posture.

Amino Acids↗
PubMed1997

Hepatic denervation induces supersensitivity to terbutaline of the hepatic arterial system in conscious dogs.

The effects of hepatic denervation on liver blood flow and the influence of the denervation on the hemodynamic response to exogenously administered agents remain equivocal. This study examined the effects of the beta 2-adrenoceptor agonist, terbutaline, on liver blood flow and how these effects were influenced by surgical hepatic denervation in a conscious canine model. Two weeks after denervation, hepatic arterial flow, portal venous flow, and aortic blood flow were measured during intravenous infusion of terbutaline at 0.1, 0.2, 0.4, and 0.8 microgram/kg/min, and responses were compared between the hepatic denervated and sham-operated dogs. Implantable transit-time ultrasonic flowmeter and probes were used. Hepatic arterial flow increased dose-dependently in response to terbutaline in denervated dogs, while it remained unchanged in control dogs except at the highest dose of terbutaline. The increase in hepatic arterial flow of denervated dogs was significantly greater than that of controls at all doses of terbutaline. Aortic blood flow-indexed hepatic arterial flow in response to terbutaline also differed substantially between the two groups. Terbutaline produced a marked dose-dependent increase of portal venous flow similarly in both groups. These results suggest that the beta 2-adrenoceptor agonist terbutaline should be effective for increasing liver blood flow and could lessen postoperative liver ischemia. We speculate that hepatic denervation induces supersensitivity of the hepatic arterial system to intravenous terbutaline.

Adrenergic beta-Antagonists↗
PubMed1998

Anticholinergic action of clonidine in rats with sinoaortic denervation.

A study was carried out relating to the anticholinergic action of clonidine on the cardiovascular responses to i.c.v. injection of neostigmine, a quaternary anticholinesterase, in conscious sham-operated animals and rats with sinoaortic denervation, 7 days after the corresponding operation. Neostigmine (0.1-1 micrograms i.c.v.) induced a dose-dependent pressor and bradycardic responses in sham-operated rats but induced only an increase in blood pressure in sinoaortic-denervated animals. However, the pressor response in sinoaortic-denervated rats was significantly greater than in sham-operated animals. Clonidine (10 micrograms kg-1 i.v.) induced a fall in mean arterial pressure in sinoaortic-denervated rats but not in sham-operated animals. Moreover, sinoaortic denervation reduced the bradycardic action of this antihypertensive drug. The anticholinesterase activity of clonidine (10 micrograms kg-1 i.v.), given 30 min previously, prevented the bradycardic action of neostigmine (0.1-1 micrograms i.c.v.) but failed to modify the pressor effect in sham-operated rats. This alpha2-adrenergic agent reduced the pressor response to i.c.v. administration of neostigmine in sinoaortic-denervated rats. Alternatively, the i.c.v. administration of clonidine (3 micrograms i.c.v.), given either 15 or 30 min before neostigmine, only prevented the bradycardic effect of the anticholinesterase (0.3 micrograms i.c.v.) in sham-operated rats but not the pressor action of this drug. In sinoaortic denervated rats, 3 micrograms of clonidine i.c.v. reduced an increase in blood pressure by i.c.v. injection of the anticholinesterase. The results suggest different central cholinergic mechanisms and different cholinergic-adrenergic interactions on the cardiovascular responses elicited by centrally injected neostigmine in sinoaortic denervated rats.

Animals↗
PubMed1989

Sustained cell proliferation in denervated skeletal muscle of mice.

Cellular proliferation in skeletal muscle was measured throughout the first 4 weeks after denervation. Twenty four mice had one leg denervated, and 4 groups of 6 of these mice were injected with tritiated thymidine once daily for 7 days, either during the first, second, third or fourth week after denervation. Autoradiographic labelling of muscle and connective tissue nuclei in denervated muscles was compared with innervated muscles from the opposite innervated legs of the same mice. Labelling of connective tissue and muscle (myonuclear and satellite cell) nuclei was significantly higher in denervated muscles, compared with innervated muscles on the unoperated side. There were no significant differences among labelling of nuclei in muscles denervated for 1, 2, 3 or 4 weeks. However, connective tissue labelling after 1 week of denervation was significantly higher than at later times. This study shows that nuclei of muscle and connective tissue cells proliferate and turnover at high levels for at least one month after denervation.

Animals↗
PubMed1995

Axonal regeneration into chronically denervated distal stump. 1. Electron microscope studies.

In this study, we have analyzed the ability of axons to regenerate into chronically denervated peripheral nerve. As an experimental rat model, the proximal end of a newly transected rat tibial nerve was sutured into chronically denervated (3 months up to 16 months) common peroneal nerve. Samples for morphological studies were collected 3 and 6 weeks after anastomosis of the tibial and common peroneal nerves. Our results showing a distinct organization of the endoneurial matrix in the chronically denervated distal stumps conformed with those from previous studies. Long cytoplasmic processes of endoneurial fibroblasts in close contact with collagen fibrils (with a diameter of 50-60 nm) surrounded areas of thin collagen fibrils (with a diameter of 25-30 nm). Remnants of Schwann cell columns (i.e., bands of Büngner) were situated in areas of thin collagen fibrils. After 12 months of denervation the majority of the Schwann cells columns were replaced by thin collagen fibrils. Successful axonal regeneration was noted in distal stumps that had been denervated for 14 and even 16 months. However, axonal regeneration diminished with prolonged denervation. The regenerating axons grew through the areas of thin collagen fibrils. The maturation and thickening of the regenerated axonal sprouts resulted in a decrease in areas of thin collagen fibrils. These results suggest that a chronically denervated nerve stump has the capacity to meet regenerating axons even after 16 months of denervation, although the progressive atrophy of Schwann cell columns impairs the likelihood of good axonal regeneration. The areas of thin collagen fibrils may act as a 'plastic' bed for successful axonal regeneration, and a study of these fibrils may provide further insight into the role of the extracellular matrix during peripheral nerve regeneration.

Anastomosis, Surgical↗
PubMed1984

Denervated frog skeletal muscle. Some electrical and mechanical properties.

The effects of denervation on several mechanical and electrical parameters of frog sartorius muscle have been investigated. In denervated muscles, there is no change in the resting potential and a relatively small change in the action potential. The first alteration in the action potential is a reduction of about 30% in the maximum rate of repolarization in muscles that have been denervated for 40 days or longer. Later, the overshoot and maximum rate of depolarization also decline. No tetrodotoxin resistant action potentials could be detected. Fibrillatory potentials were observed infrequently and in most cases in depolarized fibers. Twitch tension is significantly reduced by denervation while the tetanus tension is practically unaffected by denervation. The experiments suggest that the decline in twitch tension produced by denervation reflect a defect in some step of the excitation contraction coupling sequence. On the other hand, post-tetanic potentiation of the twitch is much larger in denervated than in control muscles. This potentiation in denervated muscles is paralleled by an increased action potential duration which returns to its pretetanic duration with a time course indistinguishable from that of the twitch potentiation.

Action Potentials↗
PubMed1986

Effects of chronic renal denervation in conscious restrained rats.

Sodium (Na), calcium (Ca), inorganic phosphate (Pi) and water excretion were measured in nondiuretic (ND) and extracellular fluid (ECF) volume expanded (VE) conscious restrained rats four weeks after denervation or sham-denervation of the left kidney. On the day of the study the animals were lightly anaesthetized with ether and the femoral vessels on one side were catheterized. Urine was collected from both kidneys. The animals were allowed to recover for 3 hours and studied in a restraining chamber. In ND animals isotonic saline containing inulin and para-amino-hippuric acid (PAH) were given at a rate of 0.067 +/- 0.002 (SE) ml/min/kg body weight (BW). In VE animals the infusion rate was 0.24 +/- 0.04 ml/min/kg BW. Kidney catecholamine content was measured after the experiments. Clearances of PAH and of inulin (GFR) were the same in both kidneys. Urine volume (V), sodium excretion (UNa V/GFR), inorganic phosphate excretion (UPi V/GFR) and calcium excretion (UCa V/GFR) were significantly higher in the denervated kidneys. Values in sham denervated kidneys were not greater than those of the right kidney. Denervation was proven by demonstrating absent or very low catecholamine content in the kidneys. The results demonstrate that: chronic renal denervation in rats leads to diuresis and natriuresis even in the conscious state, thus confirming previous results from our laboratory; such changes occur independently of the state of the ECF volume and of renal haemodynamic changes; the increased excretion of Ca++ and Pi after denervation demonstrates that renal nerves affect the reabsorption of these ions either independently or by way of their effect on sodium reabsorption. These data allow us to suggest that a renal tubular dysfunction, which was proved in anaesthetized denervated animals, can also be observed in the conscious state.

Animals↗
PubMed1998

Changes of sonographic, magnetic resonance tomographic, electromyographic, and histopathologic findings within a 2-month period of examinations after experimental muscle denervation.

This study compares sonographical, histopathological, magnetic resonance imaging (MRI), and electromyographical (EMG) findings following acute muscle denervation. We performed an experimental denervation of the supraspinatus and infraspinatus muscles on 35 New Zealand white rabbits by segment resection of the suprascapular nerve. The sonographical appearance of the supraspinatus muscle was followed and documented at short time intervals within a 2-month follow-up period. The sonographical, histopathological, and MRI changes due to denervation suggest a regular pattern. Apart from the reduction of the muscle diameter, there were considerable sonographical signs of denervation with an increase of echointensity and inhomogenicity of echotexture that appeared on day 14 after injury, and progressed continuously with time. MRI revealed a remarkable increase in signal intensity 3 weeks after denervation and reproducible T2 times. Pathological spontaneous activity on EMG could also be detected from day 14 after injury. Conventional histopathological staining methods (H&E, NADH, ATPase, basic and acid phosphatase) confirmed denervation and absence of reinnervation. The first nonspecific histopathological changes were seen 11 days after denervation in the form of moderately atrophic fibers. Typical histopathological signs of denervation appeared 3 weeks after nerve dissection. In summary, EMG, ultrasound, MRI, and histopathology each showed first abnormalities after about 2 weeks. In addition to EMG, sonography and MRI can document the course of muscle atrophy and mesenchymal abnormalities in neurogenic muscle lesions.

Animals↗
PubMed1999

Effects of denervation on energy metabolism of rat hindlimb muscles: application of (31)P-MRS and (19)F-MRS.

We studied the effects of denervation on the energy metabolism and peripheral circulation dynamics of rat hindlimb muscles during and after exercise. The sciatic nerves of male Wistar rats were cut to produce denervation. Energy metabolism was assessed by phosphorus-31 magnetic resonance spectroscopy (MRS), and circulation by fluorine-19 MRS. Exercise of rat hindlimb muscles was induced by electrical stimulation at 40 Hz. The inorganic phosphate (Pi) / ¿Pi + phosphocreatine (PCr)¿ ratio, an indicator of the energy level, was 0.795 immediately after denervation. The ratios 4 and 8 weeks after denervation were 0.870 and 0.853, respectively. The intracellular pH during the 4 min after initiation of stimulation was significantly reduced 4 and 8 weeks after denervation compared with the value immediately after denervation. The signal strength of the research perfluoro-carbon (FC-43; perfluorotributylamine) a measure of circulation dynamics, increased to 167% in controls during exercise, but an increase of only 134% was seen in rats 8 weeks after denervation. These results showed that the energy supply and circulation dynamics in denervated atrophic muscles decreased during exercise compared with findings in control muscles.

Animals↗
PubMed1978

The effect of chronic cardiac denervation on infarct size following acute coronary occlusion.

The effect of acute coronary ligation on infarct size was studied in (1) ten acute control dogs, which were non-denervated, (2) in six acutely denervated dogs in which the heart was denervated immediately prior to coronary ligation and in which intra-cardiac reflexes were pharmacologically blocked, (3) in seven chronically denervated dogs in which intrapericardial nerves were cut 2 weeks prior to ligation, and (4) in four dogs which were sham-operated 2 weeks prior to ligation. Infarct size was determined using a nitro blue tetrazolium stain for dehydrogenase activity. Infarct sizes in acute controls, acutely denervated, chronically denervated, and sham-operated hearts were 20.1, 15.0, 3.8, and 21.0 per cent of left ventricular weight, respectively. Infarct sizes in acutely and chronically denervated hearts were significantly less than in acute controls (P less than 0.05). In further studies the fluorescent stain thioflavin S was used to demonstrate that perfusion of myocardium distal to the ligation was substantially greater in chronically denervated hearts than in acute controls.

Acute Disease↗
PubMed1981

A new type of lesion-induced synaptogenesis: II. The effect of aging on synaptic turnover in non-denervated zones.

Partial denervation of the dentate molecular layer causes sprouting and reinnervation by undamaged afferents within the denervated zones of young adult animals and to a lesser extent in aged animals. We have previously reported a non-degenerative remodeling of the dentate molecular layer in areas outside the primary denervated zone of young adult rats after a unilateral entorhinal lesion. In this study, we evaluate the response of aged rats under the same conditions, to see if aged animals also respond to injury in non-denervated zones. After a unilateral entorhinal lesion, the outer two-thirds of the ipsilateral dentate molecular layer loses about 85% of its input, while the outer two-thirds of the contralateral molecular layer loses less than 5% of its input (crossed temporo-dentate path). Denervation does not occur in the inner one-third of the molecular layer on either side. Within the ipsilateral inner molecular layer, the synaptic density rapidly drops 21% in the absence of degeneration and then recovers by 10 days post-lesion, as is the case in young adult animals. On the contralateral side, young adult animals show synapse turnover similar to the ipsilateral inner molecular layer. In contrast, no significant response in the total synaptic density was observed in the non-denervated contralateral inner molecular layer or the partially denervated outer two-thirds of the contralateral molecular layer. Thus, in aged animals, synaptic turnover is restricted to the massively denervated ipsilateral side. The small loss of input to the contralateral side apparently is not sufficient to initiate quantifiable turnover of synaptic contacts. This steady-state situation may be the result of an on-going stabilization of neuronal circuitry, which may limit restoration of function after injury in aged animals.

Aging↗
PubMed1984

Spread of saphenous somatotopic projection map in spinal cord and hypersensitivity of the foot after chronic sciatic denervation in adult rat.

The left sciatic nerve was cut and ligated in adult rats (chronic denervation). Twenty-one days later the right sciatic nerve was cut and ligated (acute denervation). The somatotopic maps of the surviving intact saphenous nerves (left and right) were compared on day 21 by recording from single interneurons in the dorsal horn of the spinal cord. On the acute side saphenous mediated natural responses were observed only as far caudally as L3, while no natural responses were found in L4 and 5 (this silent zone in L4 and 5 had previously been sciatic territory). In contrast, after chronic sciatic denervation, L4 and L5 were not silent to natural stimulation as the saphenous natural responses had spread into the sciatic territory. Saphenous inputs always won the sciatic territory in L4 and L5 over competing thigh afferents after chronic sciatic denervation. Electrical stimulation of the saphenous nerve on the acute side produced unit responses all the way down to S1 (with no silent areas in L4 and 5). These electrically evoked unit responses in L4 to S1 of the acute side were called 'long range' pathways. There were no differences in 'long range' electrical responses in the acutely and chronically denervated cord. The caudal boundary for electrically evoked saphenous responses was S1 on both sides of the cord, and post stimulus histograms of unit responses were not statistically different on the two sides. Thus after chronic sciatic denervation natural responses mediated by saphenous spread caudally into sciatic territory, but electrically evoked responses did not change. Behaviorally, there was the expected spread of saphenous mediated responses from the medial toe and foot to more lateral regions after chronic sciatic denervation. Unexpectedly, there was an increase in sensitivity (hyperalgesia) of the medial toe and foot. We postulate that this increased sensitivity might be mediated by the spread of saphenous projections into L4 and L5 of the cord after chronic sciatic denervation. Perhaps post traumatic neuralgia in humans could be due to increased number of spinal cord cells responding to stimulation of the receptive field of the surviving nerve.

Animals↗
PubMed1984

Prevention of denervation atrophy in muscle: mammalian neurotrophic factor is not transferrin.

Atrophy in a denervated muscle results from the disuse caused by paralysis of the muscle, and from the loss of special neurotrophic substances. Daily injections of proteins extracted from rats' sciatic nerves have been shown to prevent the non-disuse atrophy of rats' muscles denervated for 7 days. The trophic factor from chicken sciatic nerve which stimulates differentiation in aneural chick muscle in vitro has been purified and found to be closely similar to transferrin. We undertook to determine whether the trophic properties of mammalian nerve extract on denervated rats' muscles in vivo were due to the presence of serum transferrin in the extract. Atrophy was measured as the reduction in cross-sectional areas of type IIB fibers in the extensor digitorum longus muscle. Muscles denervated for 7 days and injected daily with 1 of several doses of iron-conjugated rat transferrin exhibited a rate of atrophy equivalent to that in denervated muscles that either were not treated or were injected with saline. Denervated muscles injected with crude extract of rats' sciatic nerves had significantly less atrophy than their controls. Removal of transferrin from the crude extract by immunoaffinity chromatography did not diminish its ameliorative effects on denervated muscle. Therefore, the trophic action of mammalian nerve extract on denervated rats' muscles in vivo is not due to the presence of serum transferrin in the extract.

Animals↗
PubMed1985

Action of acrylamide on selected enzymes of energy metabolism in denervated cat peripheral nerves.

The effect of acrylamide on selected glycolytic and citric acid cycle enzymes has been studied in denervated cat sciatic nerves in vitro and in vivo. The enzyme activity of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), neuron specific enolase (NSE), succinate dehydrogenase (SDH), and lactate dehydrogenase (LDH), has been examined in saline-perfused, desheathed and denervated peroneal (P) and tibial (T) nerves from cats treated with acrylamide (15 mg/kg/day, s.c.) or vehicle for 15 days. GAPDH activity in denervated P and T nerve stumps was 2.0- and 2.3-fold higher than normal P and T nerve values. GAPDH activity in Schwann cells in denervated P and T nerves of acrylamide-treated cats was markedly reduced (56% and 61% of untreated denervated nerves, respectively). LDH and SDH activities were unaffected by acrylamide and NSE activity was absent in denervated nerve stumps. Acrylamide (0.5 and 20 mM) inhibited GAPDH activity in denervated nerve homogenates by 67% and 29%, respectively. This study demonstrates that acrylamide inhibits GAPDH in Schwann cells. The significance of GAPDH inhibition by acrylamide in denervated nerves and its relation to distal axonopathy has been discussed.

Acrylamide↗
PubMed1984

Does electrical stimulation of denervated muscle, continued after reinnervation, influence recovery of contractile function?

The study was conducted to determine if daily electrical stimulation of denervated muscle, initiated the day following crush denervation and continued for 8 weeks (i.e., 5 weeks after presumptive reinnervation), would influence denervation-associated alterations in muscle size and in situ contractile properties of rat gastrocnemius. A stimulation protocol of brief, strong, isometric contractions was designed to maximize the beneficial effects as described by previous authors. By 8 weeks after crush, unstimulated muscles were still significantly lighter in wet weight, were tetanically weaker, and showed slower isometric contractile responses in situ than controls. Denervated muscles which had been stimulated daily were heavier and tetanically stronger (the latter not different from controls) than those in the nonstimulated group. Muscle weights from groups of animals killed at 2 or 4 weeks after nerve crush indicated the major benefit of stimulation occurred during this initial 4-week period. In situ fatigue properties were unaffected by denervation or stimulation. A protocol of electrical stimulation-evoked strong contractions, initiated soon after denervation and continued after reinnervation, was effective in attenuating the strength-related, but not speed-related, changes in neuromuscular function resulting from denervation. These latter changes are presumably the result of loss of "neurotrophic influence" and/or continuous low-tension muscle activity lost as a result of denervation.

Animals↗