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PubMed1982

Similarity of acetylcholine receptors of denervated, innervated and embryonic chicken muscles. 1. Molecular species and their purification.

Acetylcholine receptors were purified to homogeneity from chicken embryonic, adult innervated and denervated muscles, by bio-specific chromatographies using immobilised alpha-neurotoxin and lentil lectin. A minimum specific activity for the pure receptor was estimated to be 6000 nmol alpha-toxin binding sites/g protein. For analysis, the receptors were radio-iodinated or tritiated to high specific radioactivity with succinimidyl-[2,3-3H]propionate. All of the iodinated protein present in the purified receptor preparation reacted with antibody against the pure acetylcholine receptor from Torpedo marmorata electric organ. In the case of all three muscle types used the same oligomeric forms were obtained. The principal form has a sedimentation coefficient of about 9 S, while a minor species (approximately 5S) was also appreciable in crude preparations of embryonic and denervated muscles. Immunization of rabbits with the homogenous receptor from chicken denervated muscle produced muscle weakness characteristic of experimental autoimmune myasthenia gravis. These antisera were equally reactive towards the receptor --125I-alpha-bungarotoxin complexes from chick innervated and denervated muscles. Likewise, the electrophoretic mobilities of the receptors (9-S form) from all three muscle types were identical, as were the isoelectric points of their complexes with 125I-alpha-bungarotoxin. Collectively, these findings and associated ones on subunit structure denote that the 9-S receptor molecules from junctional and extra-junctional area and embryonic stage of chicken muscle are indistinguishable by all criteria yet applied to them.

Animals↗
PubMed1990

Myosin heavy chain isoform composition in striated muscle after denervation and self-reinnervation.

The total content of myosin heavy chains (MHC) and their isoform pattern were studied by biochemical methods in the slow-twitch (soleus) and fast-twitch (extensor digitorum longus) muscles of adult rat during atrophy after denervation and recovery after self-reinnervation. The pattern of fibre types, in terms of ultrastructure, was studied in parallel. After denervation, total MHC content decreased sooner in the slow-twitch muscle than in the fast-twitch. The ratio of MHC-1 and the MHC-2B isoforms to the MHC-2A isoform decreased in the slow and the fast denervated muscles, respectively. After reinnervation of the slow muscle, the normal pattern of MHC recovered within 10 days and the type 1 isoform increased above the normal. In the reinnervated fast muscle, the 2B/2A isoform ratio continued to decrease. Traces of the embryonic MHC isoform, identified by immunochemistry, were found in both denervated and reinnervated slow and fast muscles. A shift in fibre types was similar to that found in the MHC isoforms. Within 2 months of recovery a tendency to normalization was observed. The results show that (a) MHC-2B isoform and the morphological characteristics of the 2B-type muscle fibres are susceptible to lack of innervation, similar to those of type 1, (b) during muscle recovery induced by reinnervation the MHC isoforms and muscle fibres shift transiently to type 1 in the soleus and to type 2A in the extensor digitorum longus muscles, and (c) the embryonic isoform of MHC may appear in the adult skeletal muscles if innervation is disturbed.

Animals↗
PubMed1996

Sarco(endo)plasmic reticulum Ca2+ pump and metabolic enzyme expression in rabbit fast-type and slow-type denervated skeletal muscles. A time course study.

Recent reports by d'Albis et al. have shown that denervation of 8-day-old rabbit fast-twitch muscle (gastrocnemius) leads to the transformation of the muscle towards a slow phenotype but the changes towards slow-type myosin isoforms and contractile properties of the muscle were temporally uncoordinated. We analyzed the time course of the effects of denervation of the gastrocnemius on the expression of the sarcoplasmic reticulum calcium pump isoforms (SERCA) and on the metabolic state of the muscle. Northern-blot analysis showed a rapid loss of the fast Ca2+ pump isoform (SERCA 1) mRNA from the denervated gastrocnemius which became of the oxidative type. The changes observed were complete as early as 35 days post-natal, i.e at the time when changes in contractile properties were previously observed. Denervation of the slow-twitch soleus led to a 50% decrease in the level of the slow Ca2+ pump isoform (SERCA 2) mRNA and was without effect on the metabolic state of the muscle. These findings extend previous results suggesting that in rabbit, continuous innervation is required for differentiation of fast-twitch muscles but is not an absolute requirement for differentiation of the slow-twitch muscle.

Animals↗
PubMedDate not supplied

Abolition of the renin-releasing action of frusemide by acute renal denervation in dogs.

1. The effects of infusions of frusemide at low (0.05-0.1 mg.kg-1.min-1) and high (0.5-2.0 mg.kg-1.min-1) rates were studied on renin secretion and urinary outputs of sodium and potassium in anaesthetized dogs in which one kidney was removed and the remaining kidney was either innervated or denervated. 2. When the kidney was innervated, low rates of infusion of frusemide did not significantly affect renin secretion if urinary volume and sodium losses were replaced. Without replacement of urinary losses, renin secretion increased at sodium deficits of 0.7-0.9 mmol.kg-1 in the presence of elevated rates of sodium and potassium excretion. 3. High rates of infusion of frusemide caused an immediate increase in renin secretion from innervated kidneys which was not related to urinary losses. 4. Denervation of the kidney increased the urinary outputs of sodium and potassium while it decreased the rate of renin secretion to one-tenth of the resting value. 5. Denervation of the kidney abolished the renin-releasing action of frusemide at both low and high infusion rates even when the sodium deficit amounted to 4.3 mmol.kg-1. 6. Constriction of the aorta producing a fall of 10-30 mmHg in perfusion pressure raised the rate of renin secretion from denervated kidneys to control levels and partially restored the renin-releasing action of frusemide at high infusion rates. 7. The findings indicate that frusemide has a site of action apart from the macula densa in mediating renin release.

Animals↗
PubMed1981

Residual catecholamines in extrinsically denervated guinea-pig ileum.

1. Concentrations of noradrenaline, adrenaline and dopamine were measured in the submucosa and myenteric plexus of innervated and extrinsically denervated guinea-pig ileum using a sensitive radioisotope enzymatic assay for catecholamines. 2. Subcellular fractionation studies indicated that the microsomal fraction obtained from both layers of the normal ileum was greatly enriched with noradrenaline compared to the total homogenate. Low levels of adrenaline and dopamine were also detected in both layers of the ileum. 3. After extrinsic denervation or pretreatment with reserpine, noradrenaline was reduced to less than 3% and could no longer be visualized histochemically. Small proportions of the adrenaline and dopamine also disappeared after extrinsic denervation. 4. The residual amounts of noradrenaline, adrenaline and dopamine present after extrinsic denervation were not sensitive to reserpine and were not concentrated in microsomal fractions suggesting that these amines are not stored as neurotransmitters in intrinsic neurons of the intestine.

Animals↗
PubMed1997

Blood pressure regulation in baroreceptor-denervated rats.

1. Arterial baroreceptor denervation produces acute hypertension, but chronically denervated animals have an average arterial pressure that is similar to that of baroreceptor intact animals. 2. Although cardiopulmonary baroreceptors and renal compensations have been suggested to mediate the restoration of a normal average arterial pressure in sino-aortic denervated rats, such mechanisms are inconsistent with the available data. 3. At present the processes involved in the restoration and long-term maintenance of a normal average arterial pressure in chronic baroreceptor denervated animals are not known. An understanding of the regulation of arterial pressure that occurs in the absence of arterial baroreceptor reflexes may provide important new insights into the mechanisms underlying the long-term regulation of arterial pressure.

Animals↗
PubMed2005

Expression of glial cell line-derived neurotrophic factor (GDNF) and GDNF family receptor alpha1 in mouse taste bud cells after denervation.

Glial cell line-derived neurotrophic' factor (GDNF) has been isolated as a neurotrophic factor that affects the survival and maintenance of central and peripheral neurons. Using immunocytochemical methods, we examined whether the taste bud cells in mouse circumvallate papillae after transection of the glossopharyngeal nerves expressed GDNF and its receptor, GDNF family receptor alpha1 (GFRalpha1). By 5 and 10 days after denervation, the number of taste buds had decreased markedly; however, the remaining taste bud cells still expressed GDNF and GFRalpha1. By 14 days after denervation, most of the taste buds had disappeared and GDNF- and GFRalpha1-immunoreactive cells were not seen. By 4 weeks after denervation, numerous TrkB-immunoreactive nerve fibers had invaded the papilla and a few taste buds expressing GDNF and GFRalpha1 had regenerated. Thus, GDNF- and GFRalpha1-immunoreactive taste bud cells after denervation vanished following the disappearance of the taste buds and reappeared at the same time as the taste buds reappeared.

Animals↗
PubMed2000

Denervation techniques.

The bladder can be denervated at several levels: centrally, at the level of the sacral nerves; peripherally, on the pelvic nerves; or in the bladder, by cutting the relevant structures, by injecting substances toxic to nerves, or by hyperbaric bladder distension. These procedures target the sensory or motor nerves to weaken or to interrupt the detrusor reflex arc. Most of the procedures introduced previously, e.g. bladder trans-section by open operation, endoscopic or transvesical phenolization, hyperbaric bladder distension, and peripheral denervation of the bladder, have now been abandoned. Although some of these techniques had a high initial success rate in abolishing detrusor overactivity and in controlling incontinence, the relapse rate within 18 months approached 100%. In the early 1950s, much of the denervation surgery was performed on sacral roots and nerves. Nowadays, sacral de-afferentiation of the bladder by dorsal sacral root rhizotomy of S2-S5, using specialized techniques, either intradurally or at the conal level, has proved to be a very effective procedure for patients with spinal cord injuries and detrusor hyper-reflexia, functional low compliance and reflex incontinence, which cannot be managed by any other means. In conclusion, although in approximately 90% of patients the symptoms of an overactive bladder will be eliminated or improved by conservative methods of treatment, bladder denervation procedures still have a place in the management of these patients. In particular, with these procedures a low-pressure bladder system can be obtained and urinary continence restored in patients with complete suprasacral spinal cord lesions.

Humans↗
PubMed1981

Effects of acute and chronic denervation on release of acetylcholinesterase and its molecular forms in rat diaphragms.

Hemidiaphragms were removed from rats at various times after intrathoracic transection of the left phrenic nerve and were incubated in organ baths containing 1.5 ml of oxygenated, buffered physiologic saline solution, with added glucose and bovine serum albumin. After incubation, the acetylcholinesterase (AChE: EC 3.1.1.7) activities of the bath fluid and of the muscle were determined. Innervated left hemidiaphragms were found to release 107 units of AChE over a 3-h period, corresponding to 1.9% of their total AChE activity. Denervation led to a rapid loss of AChE from the muscle coincident with a transient increase in the outpouring of enzyme activity into the bath fluid. Thus, 1 day after nerve transection the left hemidiaphragm contained only 68% of the control amounts of AChE activity, but released 140% as much as control. After 3 or 4 days of denervation, the AChE activity of the diaphragm stabilized at 35% of the control value. Release also fell below control by this time, but not as far. One week after denervation the release, 69 units per 3 hr, correspond to 3.3% of the reduced content of AChE activity in the muscle, indicating that denervation caused an increase in the proportion of AChE released. Sucrose density gradient ultracentrifugation showed that 10S AChE accounted for more than 80% of the released enzyme activity at all times. The results did not rule out the possibility, however, that the released enzyme originally stemmed from 4S or 16S AChE in the diaphragms.

Acetylcholinesterase↗
PubMed1982

Regeneration of cholinesterases in the stellate and normal and denervated superior cervical ganglion of the cat following inactivation by sarin.

Experiments were designed to test the hypothesis that ganglionic butyrylcholinesterase (BuChE) is derived from acetylcholinesterase (AChE). At 5 to 8 days following preganglionic denervation of the right superior cervical ganglion (SCG), cats were given sarin, 2.0 mumol/kg, i.v. At intervals of 1 h and 1, 2, 3, 6, 11, and 22 days later, they were killed, and the AChE and BuChE contents of both SCG and both stellate ganglia (StG) were assayed. The regeneration of AChE in the normal ganglia occurred in two phases: an initial rapid phase, to 25-40% of control activity in 1 day, and a slow phase, to approximately 70% of control activity in 22 days. BuChE reached approximately 85% of control activity in normal SCG and StG at 22 days. In the denervated SCG, AChE activity reached a maximum of approximately 17% of normal at 1 day, the value prior to the administration of sarin, and did not increase appreciably above this subsequently. BuChE activity in the denervated SCG reached approximately 50% of normal ganglia at 22 days. At each interval, its activity approached 55% of that of the contralateral normal SCG, the value found in the denervated SCG prior to the administration of sarin. Hence, the regeneration of BuChE appears to be independent of the presence of AChE in the neuropil. The origin of ganglionic BuChE remains obscure.

Acetylcholinesterase↗
PubMed1992

Different natures of supersensitivity of adenylate cyclase stimulated by calcitonin gene-related peptide and isoproterenol in rat diaphragm after denervation and reserpine treatment.

In skeletal muscles, calcitonin gene-related peptide (CGRP) released from motor nerve terminals and humoral catecholamines stimulate adenylate cyclase (AC) and enhance muscle contraction. The effects of denervation and treatment with reserpine on twitch contraction and the AC system in rat diaphragm were investigated. The basal levels of twitch contraction and AC activity of the diaphragm of rats were both increased 2 weeks after phrenic nerve denervation but were not altered by treatment with reserpine. Reserpine treatment provoked supersensitivity of AC to isoproterenol, without affecting the response to CGRP. On the other hand, denervation decreased the activation of AC and enhancement of twitch contraction by CGRP, without affecting the responses to isoproterenol. These data suggest that denervation causes up-regulation of AC as a result of loss of CGRP release from nerve terminal and that depletion of catecholamines by reserpine treatment supersensitizes the responses at the beta-adrenoceptor level. Thus, nervous and humoral factors regulate the AC system in striated muscle by different mechanisms.

Adenylyl Cyclases↗
PubMed1993

Comparison between the effects of botulinum toxin-induced paralysis and denervation on molecular forms of acetylcholinesterase in muscles.

Velocity sedimentation analysis of acetylcholinesterase (AChE) molecular forms in the fast extensor digitorum longus muscle and in the slow soleus muscle of the rat was carried out on days 4, 8, and 14 after induction of muscle paralysis by botulinum toxin type A (BoTx). The results were compared with those observed after muscle denervation. In addition, the ability of BoTx-paralyzed muscles to resynthesize AChE was studied after irreversible inhibition of the preexistent enzyme by diisopropyl phosphorofluoridate. Major differences were observed between the effects of BoTx treatment and nerve section on AChE in the junctional region of the muscles. A precipitous drop in content of the asymmetric A12 AChE form was observed after denervation, whereas its decrease was much slower and less extensive in the BoTx-paralyzed muscles. Recovery of junctional AChE and of its A12 form after irreversible inhibition of the preexistent AChE in BoTx-paralyzed muscles was nevertheless very slow. It seems that a greater part of the junctional A12 AChE form pertains to a fraction with a very slow turnover that is rapidly degraded after denervation but not after BoTx-produced muscle paralysis. The postdenervation decrease in content of junctional A12 AChE is therefore not primarily due to muscle inactivity. The extrajunctional molecular forms of AChE seem to be regulated mostly by muscle activity because they undergo virtually identical changes both after denervation and BoTx paralysis. The differences observed in this respect between the fast and slow muscles after their inactivation must be intrinsic to muscles.

Acetylcholinesterase↗
PubMed1987

Prolonged supersensitivity to noradrenaline of smooth muscle of the epididymal half of the rat vas deferens denervated by vasectomy.

1 The effects of some sympathomimetic amines and of carbachol and potassium chloride upon the contractility of epididymal halves of the rat vas deferens have been examined in vitro at several times following vasectomy by medial transection of the vas deferens in vivo. The inhibitory effects of noradrenaline and the excitatory effects of potassium chloride upon prostatic halves of transected tissues were also studied. 2 Partially denervated epididymal segments, taken 2 days after surgery, were spontaneously active, and responses to KCl (80 mmol/l) and maximum responses to phenylephrine were enhanced. These effects were not observed with preparations taken at later times. Spontaneous activity and enhancement of responses to KCl were abolished by guanethidine (0.1 mumol/l). 3 Supersensitivity to noradrenaline was observed in fully denervated epididymal halves of vasa deferentia taken 7-183 days after transection. The supersensitivity consisted of a leftward shift in the log concentration-response curves for noradrenaline constructed upon operated, relative to those obtained upon unoperated preparations. Supersensitivity to phenylephrine but not to methoxamine or to carbachol was also evident. 4 The magnitude of the leftward shift in the log concentration-response curve for noradrenaline in operated epididymal segments approached that produced, in unoperated segments, by nisoxetine (0.1 mumol/l). This inhibitor of neuronal uptake did not enhance the potency of noradrenaline in operated segments. 5 Prazosin (50 nmol/l) antagonized the effect of phenylephrine upon both operated and unoperated epididymal segments. The antagonism was significantly greater upon operated segments than upon unoperated segments 4 and 28 days after surgery. 6 In prostatic segments, noradrenaline produced inhibition of field stimulation-induced twitches. Its potency was similar in both operated and unoperated preparations, and nisoxetine (0.1 mumol/l) potentiated its effects to a similar extent (approximately 70-fold) in control and operated tissues. Responses to KCl in this half of the vas deferens were essentially unaffected by vasectomy. 7 Taken together, these findings indicate that post-ganglionic denervation of the epididymal half of the rat vas deferens by medial transection (vasectomy) leads to a slowly developing and prolonged supersensitivity to noradrenaline which is primarily due to the loss of the neuronal uptake facility. Persistent adaptive changes in the effector cells are apparently minimal after this means of denervation.

Adrenergic alpha-Agonists↗
PubMed1970

A comparison of the sensitivities of innervated and denervated rat vasa deferentia to agonist drugs.

1. One vas deferens of a rat was denervated by stripping away the serous coat; the other vas was left intact as a control. One week later the sensitivity in vitro of both vasa deferentia to noradrenaline, adrenaline, dopamine, oxymetazoline or acetylcholine was measured.2. Log concentration response curves for the mean responses of both vasa from a group of four rats for each drug were plotted. Denervated vasa were more sensitive than control vasa to noradrenaline (16-fold), to adrenaline (8-fold), to dopamine (2-fold) and to oxymetazoline (2-fold). Denervated vasa were more sensitive to acetylcholine over the lower half of the concentration range only.3. It is concluded that these results support the theory that at least part of the increased sensitivity of denervated smooth muscle to catecholamines is due to an abolition or reduction of the neuronal uptake process. There is also a small non-specific increase in sensitivity.

Acetylcholine↗
PubMed1973

Effects of cocaine or denervation on responses of isolated strips of cat spleen to (-)-noradrenaline and (-)-isoprenaline.

1. A study has been made of the effects of cocaine and sympathetic denervation on responses of the cat spleen to (-)-noradrenaline and (-)-isoprenaline.2. Responses of isolated strips of spleen capsule to (-)-noradrenaline or to (-)-isoprenaline were not affected by reserpine-pretreatment.3. In adult cats, cocaine (1 and 10 mug/ml) or denervation produced a shift to the left of dose-response curves to (-)-noradrenaline, whereas they failed to modify dose-response curves to (-)-isoprenaline.4. There was an increase in the maximum development of tension to (-)-noradrenaline after denervation or in the presence of cocaine (10 mug/ml). These procedures did not increase the maximal responses to (-)-isoprenaline.5. Cocaine (10 mug/ml) did not affect dose-response curves to (-)-noradrenaline or (-)-isoprenaline in the denervated spleen.6. In the kitten spleen, cocaine (1 and 10 mug/ml) produced a shift to the left of dose-response curves to (-)-noradrenaline both in untreated and in reserpine-pretreated tissues.7. There was a small shift to the left in dose-response curves to (-)-isoprenaline in the presence of cocaine in the untreated but not in the reserpine-pretreated kitten spleen.8. It is concluded that the potentiation of responses to (-)-noradrenaline in the cat's spleen is due to a prejunctional effect of cocaine.

Animals↗
PubMed1975

Desensitization in the innervated and in the chronically denervated soleus muscle of the mouse.

1 A study was made of desensitization in chronically denervated and in normally innervated mouse soleus muscles. 2 Very high concentrations of acetylcholine produced small contractions of the innervated muscles; these were reduced in size when the addition was repeated 1 min after wash-out. 3 Desensitization in innervated muscles was receptor specific: contractions in response to KCl and caffeine were not reduced following acetylcholine, nor did KCl produce desensitization. 4 In chronically denervated muscles non-specific desensitization was observed if acetylcholine was added in the presence of low concentrations of acetylcholine or carbachol. Contractions to KCl but not to caffeine were reduced. KCl produced a similar kind of desensitization. 5 After washing out moderate or supramaximal concentrations from the chronically denervated muscle no desensitization was observed. However, 1 min after washout of very high concentrations the muscle was non-specifically desensitized. 6 It is concluded that relatively high concentrations of acetylcholine are required to produce specific desensitization in the soleus muscle. Chronically denervated muscles, being supersensitive, show non-specific loss of sensitivity with concentrations of acetylcholine too low to produce specific desensitization.

Acetylcholine↗
PubMed1992

Myocardial hypertrophy, cardiac beta-adrenoceptors and adenylate cyclase activity during sinoaortic denervation in dogs.

1. The long-term effects of sinoaortic denervation on the development of left ventricular hypertrophy (assessed by the measurement of the ratio (R): heart weight/total body weight and LVT: left ventricular thickness), myocardial beta-adrenergic receptivity (measured by [125I]-cyanopindolol binding and adenylate cyclase activity) and plasma catecholamine levels (measured by h.p.l.c.) were investigated in three groups of dogs: normotensive controls (group 1), dogs made hypertensive by sinoaortic denervation and evaluated 1 (group 2) and 18 months (group 3) later. 2. Noradrenaline (NA) and adrenaline (A) plasma levels were 461 +/- 54 and 85 +/- 45 pg ml-1 in controls, 861 +/- 185 and 191 +/- 23 pg ml-1 in group 2 (P less than 0.05). They were normal in group 3 (426 +/- 132 and 110 +/- 16 pg ml-1). 3. R and LVT values were significantly (P less than 0.05) higher in sinoaortic denervated dogs (R = 7.7 +/- 0.1 and 7.8 +/- 0.2; LVT = 13.6 +/- 1.3 and 14.2 +/- 0.9 mm in groups 2 and 3 respectively) than in normotensive dogs (group 1: R = 6.7 +/- 0.1, LVT = 9.3 +/- 0.8 mm). 4. In group 1, the total number of beta-adrenoceptors (Bmax) was 37 +/- 11 and 29 +/- 6 fmol mg-1 protein in the left ventricle (LV) and right auricle (RA) respectively. In group 2, Bmax was significantly lower (10 +/- 3 in LV and 13 +/- 2 fmol mg-1 protein in RA, P less than 0.05) than in group 1. There was no difference between group 1 and group 3 (37 +/- 3 fmol mg-1 prot in LV and 31 +/- 3 fmol mg-1 protein in RA). 5. The percentage of beta 1-adrenoceptors was 82 +/- 4 in LV and 75 +/- 5 in RA in group 1. It was significantly lower (P less than 0.05) in groups 2 (LV: 33 +/- 6 and RA: 33 +/- 5) and 3 (LV: 59 +/- 3 and RA: 55 +/- 4). 6. Basal values of adenylate cyclase activity in LV significantly decreased after sinoaortic denervation.7. These data show that sinoaortic denervation is associated with left ventricular hypertrophy which appears early (1 month) and persists until 18 months despite the normalization of plasma catecholamine levels. The total number of myocardial beta-adrenoceptors is closely related to catecholamine levels but a selective decrease in beta 1-adrenoceptors is observed during cardiac hypertrophy. The fall in basal adenylate cyclase activity suggests that cardiac hypertrophy is associated with an impairment of transmembrane signalling.

Adenylyl Cyclases↗
PubMed2005

In vivo assessment of conduction velocity and refractory period of denervated muscle fibers.

Stimulation needle electromyography was used to study the muscle fiber conduction velocity and refractory period in 4 patients with long-term denervation of the lower limb muscles due to lesion of the conus cauda or cauda equina (2 untrained and 2 trained by functional electrical stimulation). In untrained patients, the results demonstrated that propagation velocity is reduced and refractory period of the muscle fiber is increased with time of denervation. The patients performing electrical stimulation training showed higher conduction velocities and reduced refractory period despite longer lasting denervation. This suggests that electrical stimulation training is effective to improve the electrical properties of the muscle fiber. Since the obtained data show a good correlation to other clinical tests and biopsy investigations, this method could serve as an additional measurement technique to specify the status of the denervated muscle. Further animal experiments and clinical studies are necessary to proof the results in comparison to more invasive established techniques.

Electric Stimulation↗