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Motor Nerves (motor + nerve)
Terms modified by Motor Nerves Selected AbstractsBlockade of the central generator of locomotor rhythm by noncompetitive NMDA receptor antagonists in Drosophila larvaeDEVELOPMENTAL NEUROBIOLOGY, Issue 1 2001Daniel Cattaert Abstract The noncompetitive antagonists of the vertebrate N -methyl- D -aspartate (NMDA) receptor dizocilpine (MK 801) and phencyclidine (PCP), delivered in food, were found to induce a marked and reversible inhibition of locomotor activity in Drosophilamelanogaster larvae. To determine the site of action of these antagonists, we used an in vitro preparation of the Drosophila third-instar larva, preserving the central nervous system and segmental nerves with their connections to muscle fibers of the body wall. Intracellular recordings were made from ventral muscle fibers 6 and 7 in the abdominal segments. In most larvae, long-lasting (>1 h) spontaneous rhythmic motor activities were recorded in the absence of pharmacological activation. After sectioning of the connections between the brain and abdominal ganglia, the rhythm disappeared, but it could be partially restored by perfusing the muscarinic agonist oxotremorine, indicating that the activity was generated in the ventral nerve cord. MK 801 and PCP rapidly and efficiently inhibited the locomotor rhythm in a dose-dependent manner, the rhythm being totally blocked in 2 min with doses over 0.1 mg/mL. In contrast, more hydrophilic competitive NMDA antagonists had no effect on the motor rhythm in this preparation. MK 801 did not affect neuromuscular glutamatergic transmission at similar doses, as demonstrated by monitoring the responses elicited by electrical stimulation of the motor nerve or pressure applied glutamate. The presence of oxotremorine did not prevent the blocking effect of MK 801. These results show that MK 801 and PCP specifically inhibit centrally generated rhythmic activity in Drosophila, and suggest a possible role for NMDA-like receptors in locomotor rhythm control in the insect CNS. © 2001 John Wiley & Sons, Inc. J Neurobiol 48: 58,73, 2001 [source] Surface Action Potential and Contractile Properties of the Human Triceps Surae Muscle: Effect of ,Dry' Water ImmersionEXPERIMENTAL PHYSIOLOGY, Issue 1 2002Yuri A. Koryak The effects of 7 days of ,dry' water immersion were investigated in six subjects. Changes in the contraction properties were studied in the triceps surae muscle. After immersion, the maximal voluntary contraction (MVC) was reduced by 18.9% (P < 0.01), and the electrically evoked (150 impulses s,1) maximal tension during tetanic contraction (Po) was reduced by 8.2% (P > 0.05). The difference between Po and MVC expressed as a percentage of Po and referred to as force deficiency was also calculated. The force deficiency increased by 44.1% (P < 0.001) after immersion. The decrease in Po was associated with increased maximal rates of tension development (7.2%) and relaxation. The twitch time-to-peak was not significantly changed, and half-relaxation and total contraction time were decreased by 5.3% and 2.8%, respectively, but the twitch tension (Pt) was not significantly changed and the Pt/Po ratio was decreased by 8.7%. The 60 s intermittent contractions (50 impulses s,1) decreased tetanic force to 57% (P < 0.05) of initial values, but force reduction was not significantly different in the two fatigue-inducing tests: fatigue index (the mean loss of force of the last five contractions, expressed as a percentage of the mean value of the first five contractions) was 36.2 ± 5.4% vs. 38.6 ± 2.8%, respectively (P > 0.05). While identical force reduction was present in the two fatigue-inducing tests, it would appear that concomitant electrical failure was considerably different. Comparison of the electrical and mechanical alterations recorded during voluntary contractions, and in contractions evoked by electrical stimulation of the motor nerve, suggests that immersion not only modifies the peripheral processes associated with contraction, but also changes central and/or neural command of the contraction. At peripheral sites, it is proposed that the intracellular processes of contraction play a role in the contractile impairment recorded during immersion. [source] Evidence for Antinociceptive Activity of Botulinum Toxin Type A in Pain ManagementHEADACHE, Issue 2003K. Roger Aoki PhD The neurotoxin, botulinum toxin type A, has been used successfully, in some patients, as an analgesic for myofascial pain syndromes, migraine, and other headache types. The toxin inhibits the release of the neurotransmitter, acetylcholine, at the neuromuscular junction thereby inhibiting striated muscle contractions. In the majority of pain syndromes where botulinum toxin type A is effective, inhibiting muscle spasms is an important component of its activity. Even so, the reduction of pain often occurs before the decrease in muscle contractions suggesting that botulinum toxin type A has a more complex mechanism of action than initially hypothesized. Current data points to an antinociceptive effect of botulinum toxin type A that is separate from its neuromuscular activity. The common biochemical mechanism, however, remains the same between botulinum toxin type A's effect on the motor nerve or the sensory nerve: enzymatic blockade of neurotransmitter release. The antinociceptive effect of the toxin was reported to block substance P release using in vitro culture systems.1 The current investigation evaluated the in vivo mechanism of action for the antinociceptive action of botulinum toxin type A. In these studies, botulinum toxin type A was found to block the release of glutamate. Furthermore, Fos, a product of the immediate early gene, c- fos, expressed with neuronal stimuli was prevented upon peripheral exposure to the toxin. These findings suggest that botulinum toxin type A blocks peripheral sensitization and, indirectly, reduces central sensitization. The recent hypothesis that migraine involves both peripheral and central sensitization may help explain how botulinum toxin type A inhibits migraine pain by acting on these two pathways. Further research is needed to determine whether the antinociceptive mechanism mediated by botulinum toxin type A affects the neuronal signaling pathways that are activated during migraine. [source] CLINICAL AND IMMUNOLOGICAL FEATURES AND RESPONSE TO IVIg IN PATIENTS WITH CLINICALLY TYPICAL MULTIFOCAL MOTOR NEUROPATHY BUT NO OVERT CONDUCTION BLOCKJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000E. Nobile-Orazio Multifocal motor neuropathy (MMN) is characterized by progressive asymmetric limb weakness usually predominant in the upper limbs associated with conduction block (CB) in motor but not sensory nerves. There are, however, occasional patients with clinically typical MMN in whom no CB can be detected. Whether these patients differ from patients with MMN and CB remains unclear. Since 1991, we have observed 24 patients with the typical clinical features of MMN. In 20 of them (14 men and 6 women), electrophysiological studies disclosed the presence of CB in at least one motor nerve. In four (all women), no evidence of CB could be detected in examined nerves even if three had some features of demyelination, including asymmetric reduction of motor conduction velocities (1 patient) or prolonged or absent F wave latencies (3 patients). Three of them had markedly reduced or absent proximal and distal CMAP amplitudes in some nerves. The mean age of onset of MMN was similar in patients with (41.5 years, range 21,70) and without CB (41.5 years, range 24,57). The mean duration of the disease at the time of our first visit was longer in patients without CB (18.5 years, range 13,25) than in those with CB (6.3 years, 3 months,25 years); only 3 patients with CB had a duration of the disease longer than 10 years. All patients without CB had a predominant or exclusive impairment of upper limbs compared with 18 (90%) of those with CB. The mean Rankin score before therapy was slightly worse in patients without (2.5) than with (2.2) CB. Anti-ganglioside antibodies were found in 1 patient without CB (25%) and in 8 (40%) with CB. All but 2 patients with CB (90%) consistently improved with IVIg. All patients without CB also improved with IVIg, but only one did so consistently. In conclusion, patients with the typical clinical presentation of MMN but no overt CB are clinically and immunologically indistinguishable from those with MMN and CB. The longer duration of the disease and frequent axonal impairment in patients without CB may explain the lower efficacy of IVIg in these patients than in those with CB. [source] Pathology is alleviated by doxycycline in a laminin-,2,null model of congenital muscular dystrophyANNALS OF NEUROLOGY, Issue 1 2009Mahasweta Girgenrath PhD Objective Congenital muscular dystrophy type 1A is an autosomal recessive disease that is caused by loss-of-function mutations in the laminin-,2 gene, and results in motor nerve and skeletal muscle dysfunction. In a previous study, we used genetic modifications to show that inappropriate induction of apoptosis was a significant contributor to pathogenesis in a laminin-,2,deficient mouse model of congenital muscular dystrophy type 1A. To identify a possible pharmacological therapy for laminin-,2 deficiency, we designed this study to determine whether treatment with minocycline or doxycycline, which are tetracycline derivatives reported to have antiapoptotic effects in mammals, would significantly increase lifespan and improve neuromuscular function in laminin-,2,deficient mice. Methods Mice that were homozygous for a targeted, inactivating mutation of the laminin-,2 gene were placed into control, minocycline-treated, or doxycycline-treated groups. Drug treatment began within 2 weeks of birth, and the progression of disease was followed over time using behavioral, growth, histological, and molecular assays. Results We found that treatment with either minocycline or doxycycline increased the median lifespan of laminin-,2,null mice from approximately 32 days to approximately 70 days. Furthermore, doxycycline improved postnatal growth rate and delayed the onset of hind-limb paralysis. Doxycycline-treated laminin-,2,deficient muscles had increased Akt phosphorylation, decreased inflammation, and decreased levels of Bax protein, terminal deoxynucleotidyltransferase,mediated dUTP nick end labeling,positive myonuclei, and activated caspase-3. Interpretation Doxycycline or other drugs with similar functional profiles may be a possible route to improving neuromuscular dysfunction caused by laminin-,2-deficiency. Ann Neurol 2008 [source] Segment-specific expression of connexin31 in the embryonic hindbrain is regulated by Krox20DEVELOPMENTAL DYNAMICS, Issue 4 2002Stefan Jungbluth Abstract Communication and interaction between cells has been shown to be important during the embryonic development of the vertebrate hindbrain, which becomes transiently subdivided into segments called rhombomeres (r). One gene family allowing intercellular communication and possibly being involved in the control of hindbrain development is the connexin family encoding gap junction channels. Here, we have characterized in detail the previously observed (Dahl et al., 1997) expression of one particular connexin gene, connexin31 (Cx31), in the mouse embryonic hindbrain and compared it with that of Cx43 and Cx36. We found transient Cx31 expression from approximately embryonic day (E) E8,E11 in two small lateral/dorsal subgroups of cells in the hindbrain. We could show that these spots of expression corresponded to r3 and r5 and that Cx31 expression in r3 and r5 was controlled by the transcription factor Krox20. In contrast, expression of Cx43 and Cx36 started later (from E9.5 and E10.5, respectively) and was confined to longitudinal stripes of expression. In addition, from E10.5,E11.5, Cx31 was expressed by a column of cells in ventral r4, most likely representing contralateral vestibulo-acoustic efferent neurons, immediately anterior to a ventral column expressing Cx36 at the same stage. From E11.5 onward, another site of Cx31 expression was detected in the boundary cap cells in the entry/exit points of all mixed sensory/motor and in the entry points of pure sensory nerves. This expression was not present in the boundary cap cells of the exit points of pure motor nerves. So far, our analysis of the hindbrain area of Cx31 -deficient embryos in terms of projections of sensory or motor neurons or in the generation or migration of neurons has not yet revealed any obvious defects. © 2002 Wiley-Liss, Inc. [source] Genes Differentially Expressed By Schwann Cells Of Motor Versus Sensory NervesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2001D Imperiale Charcot-Marie-Tooth (CMT) disease includes a heterogeneous group of inherited demyelinating peripheral neuropathies related to genetic defects of myelin-forming Schwann cells (SC). In CMT, as in other common acquired demyelinating neuropathies (Guillain Barré syndrome, chronic inflammatory demyelinating polyneuropathy), motor nerves are invariably more involved than sensory nerves. Also in transgenic mouse models of peripheral neuropathy, there is a preferential demyelination of motor districts independent of the type of genetic alteration. The basis for differential susceptibility to demyelination is unknown. The aim of this study was to identify differences in gene and protein expression that may underlie the differential susceptibility to demyelination of motor and sensory myelin-forming SC. Since spinal roots are the only portion of mammalian PNS in which motor and sensory axons are segregated, we extracted RNA from adult rat dorsal (sensory) and ventral (motor) spinal roots and compared corresponding cDNAs by an RNA fingerprint approach. Four differentially displayed bands were isolated. We first characterized the most differentially expressed band, which was highly enriched in sensory roots. Sequence analysis showed that the band encoded a portion of rat sarco/endoplasmic reticulum calcium transporting ATPase type 1 coding sequence (SERCA1). RT-PCR experiments confirmed SERCA1 enrichment in dorsal sensory roots. SERCA enzymes are ubiquitous calcium regulatory systems in muscle and non-muscle cells and SERCA1 is selectively enriched in skeletal muscle. To our knowledge, no studies have investigated SERCA isoform expression in peripheral nerve. Identification of a calcium regulatory molecule in SC is interesting, as calcium is essential for the proper structure and function of the nodal and paranodal portions of SC, as well as the myelin sheath. However, calcium homeostasis in SC is relatively unexplored. Experiments to localize SERCA1 transcript and protein in different PNS districts and to clarify its functional role in peripheral nerve are underway. [source] POSTIRRADIATION LUMBOSACRAL RADICULOPLEXOPATHY: IMPROVEMENT AFTER IMMUNE THERAPYJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000A. Bersano A delayed progressive impairment of peripheral nervous system including brachial and lumbosacral radiculoplexopathy is a well-known complication of local radiotherapy. No treatment for this infrequent complication is currently available. Recently, improvement after treatment with high dose immunoglobulin (IVIg) has been reported in some patients, suggesting either an immune-mediated inflammatory nerve damage induced by irradiation or a dysimmune neuropathy (CIDP-like) misdiagnosed as a postirradiation disease. We report on two patients who developed motor lumbosacral radiculoplexopathy several years after local radiotherapy. The first patient (ZA) is a 49 y.o. man developing a progressive proximal>distal weakness and hypotrophy of lower limbs, 20 years after radiotherapy of lumbosacral region for seminoma. Electrophysiological studies showed markedly reduced motor conduction velocities (CV) and prolonged F-wave latencies in lower limb nerves. The second patient (BF), is a 52 y.o. woman who developed progressive left brachial plexopathy and distal>proximal weakness and hypotrophy of lower limbs 12 years after a first course of toracoascellar and lumbar irradiation for Hodgkin lymphoma followed by a second course of cervicoclavicular irradiation for tumor recurrence 7 years later. Electrophysiological studies showed markedly reduced CMAP amplitudes and proportionally reduced CV in motor nerves. No sensory impairment was detected in both patients. CSF protein was elevated in both patients while cells were normal. On the assumption of a possible dysimmune origin of the disease, patient ZA underwent high dose intravenous steroid treatment, while patient BF, who had previously deteriorated after steroids, was treated with IVIg. After treatment, patient ZA became able to walk with less waddling, to rise from the floor and climb stairs without support, and to run. Improvement was less consistent in patient BF, whose right leg strength improved even if she still needed bilateral support to walk. The improvement observed in both patients supports the hypothesis that, at least in some patients, an immune-mediated mechanism may underlie postirradiation radiculoplexopathy. [source] Neurovascular Alignment in Adult Mouse Skeletal MusclesMICROCIRCULATION, Issue 2 2005SHAWN E. BEARDEN ABSTRACT Objective: Muscle blood flow increases with motor unit recruitment. The physical relationships between somatic motor nerves, which control muscle fiber contraction, and arterioles, which control microvascular perfusion, are unexplored. The authors tested the hypothesis that motor axons align with arterioles in adult skeletal muscle. Methods: Transgenic mice (C57BL/6 background, n = 5; 10 months of age) expressing yellow fluorescent protein in all motor nerves underwent vascular casting (Microfil). Excised epitrochlearis, gracilis, gluteus maximus, and spinotrapezius muscles were imaged at 380× and 760× and a computer-integrated tracing system (Neurolucida) was used to acquire 3-dimensional digital renderings of entire arteriolar and neural networks within each muscle. Results: Arteriolar networks were typically ,3-fold longer than neural networks. Nerves coursed with arterioles until terminating at motor endplates. Across muscles, proximity analyses revealed that , 75% of total nerve length (9.8,48.8 mm) lay within 200 ,m of the nearest arteriole (diameters of 15,60 , m). Conclusions: Somatic motor nerves and arterioles align closely within adult mammalian skeletal muscle. Understanding the signals governing neurovascular alignment may hold important clues for the advancement of tissue engineering and regeneration. [source] Clinical electrophysiological characterization of the acquired neuromyotonia phenotype of autoimmune peripheral nerve hyperexcitabilityMUSCLE AND NERVE, Issue 6 2006Paul Maddison MD Abstract Acquired autoimmune neuromyotonia is regarded as part of the spectrum of peripheral nerve hyperexcitability disorders. We aimed to use clinical neurophysiological measurements to study the extent, distribution, and characteristics of spontaneous motor unit potentials in 11 patients with acquired neuromyotonia. Investigations revealed that most spontaneous discharges recorded were motor unit, or partial motor unit potentials of normal size. Bursts of motor unit potentials arose more commonly from distal portions of the peripheral nerve and had abnormal absolute and relative refractory periods. Spontaneous discharges in some patients occurred in semirhythmic bursts in certain muscles. No patient had neurophysiological abnormalities detectable in first-order neurons of the central nervous system when using transcranial magnetic stimulation to estimate the threshold for corticomotor excitation and determine central motor conduction time. Only patients with coexistent myasthenia gravis had neurophysiologically detectable defects in neuromuscular transmission. The pathogenic region of abnormality in peripheral nerve hyperexcitability disorders therefore seems to lie within the terminal branches of peripheral motor nerves. Muscle Nerve, 2006 [source] Capsaicin delays regeneration of the neuromuscular junction of rat extensor digitorum longus muscle after ischemiaMUSCLE AND NERVE, Issue 4 2006Béla Turchányi MD Abstract Trauma or the tourniquet used in orthopedic surgery is often associated with ischemia,reperfusion (I/R) injury with a consequent decrease of muscle power. To explore whether components of the neuromuscular junction (NMJ) are involved in this muscle dysfunction, NMJs were ultrastructurally characterized in the extensor digitorum longus muscle of rats at reperfusion times of 1, 24, 72, and 168 h after a 120-min arterial occlusion. Disorganization of the presynaptic membrane and mitochondrial injury was noted at 1 h, followed by fragmentation and partial engulfment of nerve terminals by Schwann cells at 24 and 72 h. The magnitude of degenerative changes declined at 168 h, suggesting the commencement of regeneration. The postsynaptic membrane remained intact throughout the whole period. In our previous study, deafferentation with pretreatment of the sciatic nerve with capsaicin, which reduces neurogenic inflammation and has a selective effect on nociceptive fibers, improved functional recovery of the muscle after I/R. The present results document a significantly delayed structural regeneration of the motor nerve terminals after combined capsaicin and I/R treatment. Since capsaicin treatment alone had no discernible effect on the structure of NMJs, the findings point to a possibly indirect effect of capsaicin on the motor nerves, which may predispose them to increased susceptibility unmasked only by a subsequent injury. The mismatch between the enhanced functional improvement of the muscle and delayed regeneration of the nerve after capsaicin pretreatment questions the efficient use of such deafferentation to protect the integrity of neuromuscular junctions in I/R injury. Muscle Nerve, 2006 [source] Phenol Neurolysis for Severe Chronic Nonmalignant Pain: Is the Old also Obsolete?PAIN MEDICINE, Issue 4 2007Natan Weksler MD ABSTRACT Objective., Our purpose was to reassess the effectiveness of phenol 4% in aqueous solution for neurolysis in patients with severe chronic nonmalignant pain syndromes who did not achieve adequate pain control (visual analog scale [VAS] ,3) with conventional pain treatment. Design., Forty-two patients with severe nonmalignant pain persisting for 6 months or longer were followed for more than 6 months after phenol neurolysis in this prospective observational study. All patients had previously received narcotic drugs, with or without nonsteroidal anti-inflammatory agents or adjuvants, without adequate pain relief. An aqueous solution of phenol 4% was used for chemical neurolysis. A fluoroscopically guided technique was used for chemical lumbar sympathectomy, medial branch destruction, and sacroiliac injections. Anatomic-landmarks technique was used for intercostal neurolysis, greater occipital nerve destruction, genitofemoral neuroablation, and paracoccygeal infiltration. Results., Good pain relief (VAS ,3) was achieved in 35 patients after neurolysis with phenol, and the mean VAS decreased from 8.74 ± 1.08 (range 7,10) before treatment to 1.93 ± 2.41 after treatment (P < 0.0001). The mean VAS for assessment of the quality of pain relief after phenol neurolysis was 8.4 ± 2.39, ranging from 0 (no relief at all) to 10 (complete relief ). No major complications were seen. Conclusion., The use of phenol 4% in aqueous solution is an effective and safe technique for neurolysis. Because of the potential risk of flaccid paralysis, this technique should be used in selected cases, far removed from motor nerves and the spinal cord. [source] Synaptic specializations exist between enteric motor nerves and interstitial cells of Cajal in the murine stomachTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2005Elizabeth A.H. Beckett Abstract Autonomic neurotransmission is thought to occur via a loose association between nerve varicosities and smooth muscle cells. In the gastrointestinal tract ultrastructural studies have demonstrated close apposition between enteric nerves and intramuscular interstitial cells of Cajal (ICC-IM) in the stomach and colon and ICC in the deep muscular plexus (ICC-DMP) of the small intestine. In the absence of ICC-IM, postjunctional neural responses are compromised. Although membrane specializations between nerves and ICC-IM have been reported, the molecular identity of these specializations has not been studied. Here we have characterized the expression and distribution of synapse-associated proteins between nerve terminals and ICC-IM in the murine stomach. Transcripts for the presynaptic proteins synaptotagmin, syntaxin, and SNAP-25 were detected. Synaptotagmin and SNAP-25-immunopositive nerve varicosities were concentrated in varicose regions of motor nerves and were closely apposed to ICC-IM but not smooth muscle. W/WV mice were used to examine the expression and distribution of synaptic proteins in the absence of ICC-IM. Transcripts encoding synaptotagmin, syntaxin, and SNAP-25 were detected in W/WV tissues. In the absence of ICC-IM, synaptotagmin and SNAP-25 were localized to nerve varicosities. Reverse transcriptase polymer chain reaction (RT-PCR) and immunohistochemistry demonstrated the expression of postsynaptic density proteins PSD-93 and PSD-95 in the stomach and expression levels of PSD-93 and PSD-95 were reduced in W/WV mutants. These data support the existence of synaptic specializations between enteric nerves and ICC-IM in gastric tissues. In the absence of ICC-IM, components of the synaptic vesicle docking and fusion machinery is trafficked and concentrated in enteric nerve terminals. J. Comp. Neurol. 493:193,206, 2005. © 2005 Wiley-Liss, Inc. [source] Modifying techniques in deep inferior epigastric artery perforator flap harvest with the use of preoperative imagingANZ JOURNAL OF SURGERY, Issue 9 2009Warren M. Rozen Abstract New techniques in the harvest of deep inferior epigastric artery perforator (DIEP) flaps have become introduced as a result of modern imaging technologies that can allow virtual surgery to be achieved preoperatively. With computed tomographic angiography, individual anatomy can be appreciated in detail to a level not previously appreciated. These imaging techniques can be successfully used to guide DIEP flap surgery. ,Optimal' perforators can be selected based on size, location, intramuscular and subcutaneous course, and their association with motor nerves. Flap design can be safely achieved based on the cutaneous distribution of perforators. Abdominal wall closure can be improved based on the abdominal contour seen with imaging. Preoperative planning can aid patient selection, plan all aspects of the operative technique, reduce operating time and improve operative outcomes. [source] | |||||||||||||