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PubMed1991

Cyclic AMP stabilizes the degradation of original junctional acetylcholine receptors in denervated muscle.

We used mouse diaphragm muscle in organ culture to study the stabilization of acetylcholine receptor (AChR) degradation at denervated neuromuscular junctions. After denervation, the degradation rate of the AChRs present prior to denervation (slowly degrading, or Rs, AChRs) accelerates from the predenervation degradation half-life (t1/2) of approximately 8-10 days to a t1/2 of approximately 2-3 days. We report that addition to the organ culture medium of pharmacological agents that elevate cytoplasmic cAMP levels (forskolin, dibutyryl cAMP, and 8-bromo-cAMP) reversed the change in t1/2 caused by denervation, whereas addition of 1,9-dideoxyforskolin, a forskolin analog that does not elevate cytoplasmic cAMP levels, did not reverse the effect of denervation. The degradation rate of AChRs in primary myotube cultures and that of the newly synthesized AChRs in denervated muscle were little affected by forskolin or dibutyryl cAMP. The possibility is raised that the modulation of Rs AChR degradation by innervation may be mediated by cAMP.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2004

Transplanted neural stem cells promote axonal regeneration through chronically denervated peripheral nerves.

Regeneration in the peripheral nervous system is impaired after prolonged periods of denervation. Currently, no interventions exist to alter the outcome after prolonged denervation. To examine the role of transplanted neural stem cells (NSC), we prepared chronically denervated distal tibial nerve segments. After 6 months of chronic denervation, we transplanted vehicle, C17.2 mouse NSCs, or C17.2 mouse NSCs engineered to overexpress GDNF to the distal tibial nerve and performed a peroneal nerve cross-suture. In animals transplanted with the NSCs, there was better regeneration of the peroneal axons into the tibial nerve as measured by counting the number of axons and by the emergence of compound motor action potentials in the tibial innervated foot muscles. Improved regeneration correlated with a reduction of chondroitin sulphate proteoglycan (CSPG) immunoreactivity in the extracellular matrix (ECM). In vitro, supernatant from C17.2 NSCs contained large quantities of secreted matrix metalloprotease-2 (MMP-2), degraded the CSPGs on chronically denervated tibial nerve sections, and reversed the CSPG-induced inhibition of neuritic outgrowth of DRG neurons. This reversal was inhibited by selective MMP-2 inhibitors. This is the first successful demonstration of regeneration through a chronically denervated nerve. These findings suggest that improved regeneration in the PNS can be accomplished by combining neurotrophic factor support and removal of axon growth inhibitory components in the extracellular matrix.

Action Potentials↗

PubMed2005

Pro- and anti-apoptotic evidence for cholinergic denervation and hippocampal sympathetic ingrowth in rat dorsal hippocampus.

In rat, injection of the specific cholinotoxin, 192 IgG-saporin, into the medial septum results not only in a selective cholinergic denervation of hippocampus, but in an ingrowth of peripheral sympathetic fibers, originating from the superior cervical ganglion, into the hippocampus. A similar process, in which peripheral noradrenergic axons invade hippocampus, may also occur in Alzheimer's disease. Since apoptotic cell death has been demonstrated in the selective neuronal loss found in Alzheimer's disease, the aim of this study was to measure apoptotic protein expression and DNA fragmentation in hippocampal sympathetic ingrowth and cholinergic denervation. Western blot, TdT-mediated dUTP nick end labeling, and oligo ligation techniques were used. Choline acetyltransferase activity and norepinephrine concentrations were also measured. As seen in our previous results, an increase in apoptotic markers was induced by cholinergic denervation alone (medial septum lesion + ganglionectomy), while hippocampal sympathetic ingrowth (medial septum + sham ganglionectomy) reduced or normalized apoptotic effects to control group levels. A decrease in choline acetyltransferase activity was also found in the dorsal hippocampus of hippocampal sympathetic ingrowth and cholinergic denervation groups. An increase in norepinephrine concentration was found in hippocampal sympathetic ingrowth but not in cholinergic denervation group. Results of this study suggest that cholinergic denervation is responsible for most of the proapoptotic responses, while hippocampal sympathetic ingrowth produces a protective effect in the process of programmed cell death in rat dorsal hippocampus. This effect may be a secondary to an altered relationship between norepinephrine-acetylcholine.

Acetylcholine↗

PubMed2005

In vivo complete neural isolation of the rat jejunoileum: a simple model to study denervation sequelae of intestinal transplantation.

BACKGROUND: Our aim was to develop and validate a technically easy, reliable, and reproducible method of complete jejunoileal denervation in the rat to allow study of the physiologic effects of intestinal transplantation devoid of immunologic phenomena and ischemia/reperfusion injury. MATERIALS AND METHODS: Six adult Sprague-Dawley rats underwent transection and reanastomosis of the proximal jejunum and proximal colon, transection of all neurolymphatic tissues at the base of the mesentery, stripping adventitia off the superior mesenteric artery and vein, and radial transection of the intervening mesenteries, thereby denervating the jejunoileum in situ without disrupting blood flow. Three rats each were sacrificed 1 and 6 months later. Intestinal smooth muscle from the still-innervated duodenum and the denervated jejunum, mid-small bowel, and ileum was compared to corresponding tissues from a normal rat for tyrosine hydroxylase immunohistochemistry, a marker of extrinsic innervation. RESULTS: One and six months after denervation, all duodenal samples demonstrated normal tyrosine hydroxylase immunostaining. In contrast, tyrosine hydroxylase immunoreactivity was undetectable in jejunum, mid-small bowel, or ileum of rats at 1 month and 2 of the 3 rats at 6 months; 1 rat at 6 months had low levels of tyrosine hydroxylase immunoreactivity at the mesenteric border of jejunum and mid small bowel. CONCLUSION: This simple technique of in situ neural isolation effectively and reproducibly achieves complete extrinsic denervation of the entire rat jejunoileum. Low levels of neural regeneration may be present 6 months after denervation.

Animals↗

PubMed2005

Quantitative ultrastructural changes in satellite cells of rats immobilized after soleus muscle denervation.

Quantitative ultrastructural evaluation of satellite cells (SCs) of rats immobilized for 7, 14, and 36 days after soleus muscle denervation was performed. Alterations in SCs of experimental animals concerned mainly the decrease in the size of cells and their nuclei, in the volume fractions of the nucleus and nucleolus, as well as in the number of ribosome-like structures. They suggest that immobilization which proceeded denervation caused a decline in cell activity. An increase in the volume fraction and number of endosome/lysosome-like structures, suggesting elevated processes of degradation was also observed. The changes occurred mainly in the period between 7 and 14 days after muscle denervation and immobilization. In all groups of experimental animals an increase in number of caveolae-like structures on both, inner (muscle fiber-facing) and outer (basal lamina-facing) sides of SCs was found. Thus, it is likely that SCs of denervated and immobilized rats are affected by signal molecules released by muscle fibers and/or other cell types present in muscle. A tendency in changes in SCs, observed in the present study, was similar to those which we noticed previously in denervated soleus muscle. However, immobilization after denervation aggravated some of the ultrastructural alterations or the changes appeared earlier.

Animals↗

PubMed1998

[Joint denervation, a simple response to complex problems in hand surgery].

STUDY AIM: In patients with preserved mobility and stability a painful joint remains a difficult problem, especially in elderly patients. All operations, including intracarpal arthrodesis, reduce an already limited mobility, require prolonged immobilization and have a high rate of complications. Denervation could be proposed in such cases. MATERIALS AND METHODS: In our study denervation was performed on 132 wrists, 36 first carpo-metacarpal joints and 32 proximal inter-phalangeal joints. RESULTS: We have been disappointed in the past by partial wrist denervations. Fifty cases of complete and isolated wrist denervation were reviewed with a mean 5-year followup. Strength and mobility were only marginally improved but pain was decreased by a mean 75% (on a visual analog scale) in 74% of patients. At the proximal inter-phalangeal joint level, the mean pain improvement was 88% in 85% of patients. At the first carpo-metacarpal joint level, results of denervation were less predictable and the mean pain improvement was 67% in 81% of patients, with a mean 17-month follow-up. CONCLUSION: Joint denervation is a simple but precise operation performed under local anesthesia and on an outpatient basis. It provides good results in elderly patients, with few complications.

Adult↗

PubMed1981

Protective effect of chronic versus acute cardiac denervation on contractile force during coronary occlusion.

The effects of acute coronary artery (CA) occlusion on myocardial contractile force were studied in mongrel dogs with (1) chronically denervated hearts (n = 10), (2) acutely denervated hearts (n = 5), and (3) normally innervated hearts (n = 6). Contractile force was measured in ischemic and nonischemic areas using Walton-Brodie strain gauge arches sutured to the epicardium. Coronary occlusion was accomplished by ligating several small branches of the left anterior descending and the circumflex arteries supplying the apical region on the left ventricle. Following occlusion, contractile force in the ischemic area decreased by 66.8% in the control group, by 73.6% in the acutely denervated group, but only by 21.6% (P less than 0.001) in the chronically denervated group. These results demonstrate that chronic cardiac denervation protects from the severe loss of contractile force in the ischemic area. This salutary effect is not seen with acute cardiac denervation.

Animals↗

PubMed1999

Loss of regulation by presynaptic dopamine D2 receptors of exogenous L-DOPA-derived dopamine release in the dopaminergic denervated striatum.

To determine whether dopamine release derived from exogenous l-DOPA is under inhibitory control of presynaptic dopamine D2 receptors in the dopaminergic denervated striatum, extracellular dopamine levels were measured in the striatum of 6-hydroxydopamine-lesioned rats using in vivo brain microdialysis. Quinpirole, a D2 agonist, dose-dependently (0.01-3 mg/kg s.c.) inhibited endogenous dopamine release both in the intact and dopaminergic denervated striatum. The dose-response curve obtained from the denervated striatum showed a shift to the right. Administration of l-DOPA (30 mg/kg i.p.) with carbidopa (25 mg/kg i.p.) increased dopamine release to 130% of basal levels in the intact striatum and 770% of basal levels in the denervated striatum. In the intact striatum, dopamine release was continuously inhibited by quinpirole pretreatment (1 mg/kg s.c.) even after l-DOPA administration. In the denervated striatum, l-DOPA-derived dopamine release was not affected by quinpirole pretreatment. These results suggest that, in the striatum with dopaminergic denervation, regulation by presynaptic D2 receptors is still operative on endogenous dopamine release but it does not work on dopamine release derived from exogenously administered l-DOPA.

Animals↗

PubMed1999

Influence of denervation on neurogenic inhibitory response of corpus cavernosum and nitric oxide synthase histochemistry.

Aims of this study were to functionally and histologically determine the localization of ganglia that distribute inhibitory nerves to the penile corpus cavernosum in dogs. In isolated corpus cavernosa from seven control dogs contracted with endothelin-1, transmural electrical stimulation (5 Hz for 40 s) elicited contractions which were reversed to relaxations by prazosin. The relaxation was abolished by NG-nitro-l-arginine (l-NNA), a nitric oxide (NO) synthase inhibitor, and restored by l-arginine. Parts of bilateral pelvic nerve plexuses running to the penis were surgically denervated in anesthetized three dogs, or the bilateral neuronal tissues close to the corpus cavernosum were removed for denervation in seven dogs. One week after the operation, the dogs were sacrificed. Denervation of pelvic plexus did not attenuate neurogenic relaxations, whereas denervation of the distal portion abolished the responses. In the tissues close to the corpus cavernosum excised for denervation, ganglia containing abundant nerve cells and fibers stained by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase method were histochemically detected. One week after the denervation, there were no NADPH diaphorase-positive nerve fibers in the trabecula of corpus cavernosum. It is concluded that neurogenic relaxations of canine corpus cavernosum are mediated by NO synthesized from l-arginine in nerve terminals, and this nerve is originated from ganglia located close to the corpus cavernosum but not directly from the pelvic nerve plexus.

Adenosine Triphosphate↗

PubMed1984

Indentations in the terminal cisternae of denervated rat EDL and soleus muscle fibers.

The effects of denervation on the structure of the triad and longitudinal sarcoplasmic reticulum have been investigated in freeze-fracture replicas of extensor digitorum longus (EDL) and soleus fibers that had been denervated for 2 to 70 days. In EDL fibers the density of indentations along 1 micron of terminal cisternae fell during the first 2 weeks after nerve section, from a normal value of 7.3 +/- 0.2 (mean +/- 1 SEM) to an average value of 2.0 +/- 0.5 in fibers denervated for 16 to 17 days. Denervation did not change the numbers of indentations in soleus fibers. There was a significant change in the orientation of the triads and organization of the longitudinal sarcoplasmic reticulum in denervated EDL and soleus fibers. The effect of denervation on the density of indentations was best correlated with the effect on asymmetric charge movement, when indentation density was compared with twitch contraction time, the voltage sensitivity of tension, and charge movement. The close relationship between indentation density and charge movement provides compelling evidence for a functional link between the two during excitation-contraction coupling.

Animals↗

PubMed1999

Reduced glycogen phosphorylase activity in denervated hindlimb muscles of rat is related to muscle atrophy and fibre type.

Changes in the activity of muscle glycogen synthase or phosphorylase (GP) may be responsible for the deregulation of glycogen synthesis and storage which occurs in diabetes mellitus. To clarify the relationship between muscle atrophy, fibre type, insulin-stimulated glucose uptake and GP activity during insulin resistance, we used sciatic nerve severance to induce insulin resistance in rat hindlimb muscles and compared the above parameters in muscles with a range of fibre types. Changes were analysed by comparison with the contralateral hindlimb, which bears more weight due to denervation of the opposing limb, as well as the sham-operated and contralateral limb of a separate rat. Denervation caused a decrease in insulin-stimulated glucose uptake by 1 day after denervation and a decline of GP activity after 7 days in all muscles investigated. GP activity decreased by 73% in soleus, 36% in red gastrocnemius, 35% in tibialis and 13% in white gastrocnemius, which was related to the degree of muscle atrophy and inversely related to the overall GP activity in non-denervated muscles. GP activity in muscles of the contralateral limb from the denervated rat did not differ from either hindlimb of the sham-operated rat. We conclude that the fibre-type related reduction in insulin-stimulated glucose uptake of denervated muscle determines the change in its metabolism and it is this metabolic change which determines the mechanism, rate and degree of muscle atrophy, which is directly related to the decline in GP activity.

Animals↗

PubMed2000

Reactive astrocytic responses to denervation in the motor cortex of adult rats are sensitive to manipulations of behavioral experience.

Recent research has suggested that mild denervation of the neocortex of adult rats may facilitate neuronal growth in response to behavioral changes. Astrocytes react to denervation, produce growth-promoting factors and are a potential mediator of this denervation-facilitated growth. The present study assessed whether astrocytic reactions to denervation vary dependent upon post-injury behavioral experience. Denervation of the transcallosal afferents to the motor cortex was induced via partial transections of the corpus callosum. Transected- or sham-operated rats were then either forced to use the opposite forelimb (via limb-restricting vests) or permitted to use both forelimbs normally for 8 days. In the motor cortex, the surface density of glial fibrillary acidic protein (GFAP)-immunoreactive (IR) astrocytic processes and the density of basic fibroblast growth factor (FGF-2)-IR glial cells was significantly increased as a result of transections alone and as a result of forced forelimb-use alone in comparison to controls. The combination of transections and forced-use significantly enhanced GFAP-IR in comparison to all other groups, but did not further enhance FGF-2-IR. These findings are consistent with behavior and denervation having interactive influences on astrocytic reactivity in the motor cortex. These results also raise the possibility that astrocyte-mediated support of neural restructuring after brain injury might be enhanced with appropriate post-injury behavioral manipulations.

Animals↗

PubMed2003

Improved sphincter contractility after allogenic muscle-derived progenitor cell injection into the denervated rat urethra.

OBJECTIVES: To study the physiologic outcome of allogenic transplant of muscle-derived progenitor cells (MDPCs) in the denervated female rat urethra. METHODS: MDPCs were isolated from muscle biopsies of normal 6-week-old Sprague-Dawley rats and purified using the preplate technique. Sciatic nerve-transected rats were used as a model of stress urinary incontinence. The experimental group was divided into three subgroups: control, denervated plus 20 microL saline injection, and denervated plus allogenic MDPCs (1 to 1.5 x 10(6) cells) injection. Two weeks after injection, urethral muscle strips were prepared and underwent electrical field stimulation. The pharmacologic effects of d-tubocurare, phentolamine, and tetrodotoxin on the urethral strips were assessed by contractions induced by electrical field stimulation. The urethral tissues also underwent immunohistochemical staining for fast myosin heavy chain and CD4-activated lymphocytes. RESULTS: Urethral denervation resulted in a significant decrease of the maximal fast-twitch muscle contraction amplitude to only 8.77% of the normal urethra and partial impairment of smooth muscle contractility. Injection of MDPCs into the denervated sphincter significantly improved the fast-twitch muscle contraction amplitude to 87.02% of normal animals. Immunohistochemistry revealed a large amount of new skeletal muscle fiber formation at the injection site of the urethra with minimal inflammation. CD4 staining showed minimal lymphocyte infiltration around the MDPC injection sites. CONCLUSIONS: Urethral denervation resulted in near-total abolishment of the skeletal muscle and partial impairment of smooth muscle contractility. Allogenic MDPCs survived 2 weeks in sciatic nerve-transected urethra with minimal inflammation. This is the first report of the restoration of deficient urethral sphincter function through muscle-derived progenitor cell tissue engineering. MDPC-mediated cellular urethral myoplasty warrants additional investigation as a new method to treat stress urinary incontinence.

Animals↗

PubMed1998

Increased activity improves recovery of partially denervated fast rat muscles.

Partial denervation of the neonatal rat extensor digitorum longus muscles by removing the L4 spinal nerve and thus 80% of its innervation [A.L. Connold, T.J. Fisher, S. Maudarbocus, G. Vrbová, Response of developing fast muscles to partial denervation, Neuroscience 46 (1992) 981-988; F. Tyc, G. Vrbová, The effect of partial denervation of developing rat fast muscles on their motor unit properties, J. Physiol. 482 (1995) 651-660] results in its permanent weakness. The possibility that the weakness that follows partial denervation is due to the effects of reducing activity of the muscle during a critical stage of development was studied here. Partial denervation was carried out in 3-day-old pups by removing the L4 spinal nerve. To enhance motor activity two days later some animals had injections of l-Dopa twice a day for 8 days. This treatment induced locomotor activity for at least 2 h/day. The muscles from treated and untreated animals were examined 2 months later. There was a significantly smaller reduction of weight and force production in the muscles from l-Dopa treated animals. Both twitch and tetanic force developed by the EDL muscle from the treated group was twice that of the control untreated group. This effect was due mainly to the larger size of the motor units (MUs) in the l-Dopa treated muscles compared to the controls. The mean motor unit force in the untreated group was 69% of that in the control muscle, whereas this value was 127% in the l-Dopa treated animals. Thus it appears that the activity induced by treatment with l-Dopa could to some extent prevent the loss of weight and force output seen after partial denervation of young fast muscles.

Animals↗

PubMed1997

Effect of sciatic denervation on cell-mediated immunity.

Local semiallogenic graft-versus-host (GvH) and host-versus-graft (HvG) reactions were induced in mice whose right hind limbs had been partially denervated surgically. The denervation was performed by removing a 2 mm segment of the sciatic nerve, while sham-operated and non-operated mice served as controls. Eight days after denervation the mice were injected with spleen cells from a 3-month-old C57BL female, or from (C57xCBA)F1 male mice, and the GvH and HvG reactions were evaluated, 7 or 10 days later, by quantitatively estimating the weight (enlargement) of the popliteal lymph-nodes. Significant weight increases of 51% (for the GvH reaction) and 63% (for the HvG reaction) were observed in the denervated mice, when compared to the sham-operated ones. This increased cell-type reactivity in a denervated limbs seems to be related to the immunostimulatory activity of cytokines which are released by cells engaged in repair processes of damaged nerves, as well as related to the reduction of the immunosuppressive effect of noradrenergic innervation in the denervated animals.

Adoptive Transfer↗

PubMed1998

GDNF expression is increased in denervated human skeletal muscle.

Glial cell line derived neurotrophic factor (GDNF) is a potent trophic factor for several subpopulations of neurons including motor neurons. Two different transcripts of the GDNF gene (GDNF633 and GDNF555) have been detected in various tissues, including skeletal muscle. Denervation leads to an upregulation of GDNF633 in rat skeletal muscle, indicating that GDNF is involved in the response of skeletal muscle to denervation and possibly in reinnervation. To determine the role of GDNF in human neuromuscular disease, we investigated the expression of both transcripts in normal and denervated muscle and in muscle biopsies from Duchenne muscular dystrophy patients. GDNF expression levels were analyzed by competitive RT-PCR in 38 muscle specimens. Levels of both transcripts were significantly elevated in denervated muscle compared to normal and dystrophic muscle. Morphometric analysis of muscle-fiber calibers and its correlation to GDNF expression revealed that higher levels of GDNF were expressed in rapidly-progressive neurogenic atrophy, including four amyotrophic lateral sclerosis (ALS) cases, compared to cases of chronic atrophy. In dystrophic muscle, transcript levels were not significantly altered compared to normal controls. These data indicate that denervation, but not dystrophy, enhances GDNF expression in human skeletal muscle. Thus, the increase of GDNF expression is part of the reaction of human skeletal muscle to denervation caused by motor nerve lesion. GDNF might act on regenerating nerve fibers during muscle fiber reinnervation.

Cells, Cultured↗

PubMed1999

Long-term denervation modulates differentially the accumulation of myogenin and MRF4 mRNA in adult Xenopus muscle.

In adult Xenopus laevis, we analyzed, using reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization, the influence of long-term muscle denervation on the accumulation of MRF4 and myogenin transcripts. The brachial muscle was denervated by cutting the brachial nerve and was examined after 4 months. MRF4 mRNA levels decreased about two-fold in denervated muscle as compared with contralateral muscle. Myogenin mRNA levels, by contrast, were induced about five-fold by denervation. This report shows that muscle denervation persistently reduces the levels of MRF4 transcripts suggesting that MRF4 expression may be induced by innervation and hence may be involved in mediating transcriptional responses to innervation. The up-regulation of myogenin by denervation suggests that myogenin expression may compensate for the down-regulation of MRF4 gene.

Animals↗

PubMed2000

L-DOPA produces strong induction of c-fos messenger RNA in dopamine-denervated cortical and striatal areas of the common marmoset.

Common marmosets (Callithrix jacchus) with near-complete unilateral 6-hydroxydopamine denervation of the dopaminergic input received a single injection of saline or L-DOPA (15mg/kg plus 6.25mg/kg benserazide). Using in situ hybridization, the effects of these treatments on c-fos messenger RNA expression in the cerebral cortex, the striatal complex and the external layer of the pallidum were studied. Moreover, receptor autoradiography was used to determine the levels of dopamine D(1) and D(2) receptors in these areas. In the cerebral cortex, animals treated with L-DOPA displayed a high expression of c-fos messenger RNA restricted to the dopamine-denervated hemisphere. No changes in the levels of cortical D(1) and D(2) receptors were found in the dopamine-denervated hemisphere. L-DOPA treatment also induced a strong expression of c-fos messenger RNA in the striatal complex in the dopamine-denervated hemisphere. The levels of striatal D(2), but not D(1), receptors were increased in the dopamine-denervated hemisphere. In the external pallidum, the major terminal region for D(2) dopamine receptor-containing striatal projection neurons, L-DOPA treatment induced c-fos messenger RNA expression in both the intact and the dopamine-denervated hemispheres.Thus, using c-fos messenger RNA as a biochemical marker of postsynaptic neuronal activation, these results provide evidence that near-complete dopamine depletion causes a profound supersensitization to L-DOPA treatment in the cerebral cortex and in the striatal complex, but not in the external layer of the pallidum, of the primate brain. The cortical response may be unique to the primate brain, but c-fos messenger RNA activation within the striatum has also been reported in the rodent. The effects of L-DOPA probably depend both on a direct activation of supersensitized dopamine receptors by dopamine produced in the few remaining, but hyperactive, dopaminergic nerve terminals and in serotonergic nerve terminals, as well as on indirect actions of L-DOPA related to activation of circuitries connecting cerebral cortex and basal ganglia structures. These results provide novel information on the mechanisms underlying L-DOPA's action in the cerebral cortex, striatum and external pallidum in a primate model of Parkinson's disease.

Animals↗