Motoneuron
Mostrando 13-24 de 85 artigos, teses e dissertações.
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13. Apoptose de neuronios motores, interneuronios e neuronios sensitivos induzida pela transecção do nervo ciatico em ratos recem nascidos : padrão temporal e efeitos do tratamento com fatores neurotroficos (NGH e CNTF)
Transection of a peripheral nerve in neonatal rats induces an extensive death of axotomized neurons. We demonstrate here that spinal motoneurons and sensory dorsal root ganglia neurons become TUNEL-labeled (tenninal deoxynuc1eotidyl transferase dUTP nick end labelling) afier sciatic nerve transection in neonatal rats, thus indicating that apoptotic mechanism
Publicado em: 1999
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14. Gene targeting of Gemin2 in mice reveals a correlation between defects in the biogenesis of U snRNPs and motoneuron cell death
Neuronal degeneration in spinal muscular atrophy is caused by reduced expression of the survival motor neuron (SMN) protein. SMN and the tightly interacting Gemin2 form part of a macromolecular complex (SMN complex) that mediates assembly of spliceosomal small nuclear ribonucleoproteins (U snRNPs). We used mouse genetics to investigate the function of this c
The National Academy of Sciences.
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15. Motoneuron survival is promoted by specific exercise in a mouse model of amyotrophic lateral sclerosis
Several studies using transgenic mouse models of familial amyotrophic lateral sclerosis (ALS) have reported a life span increase in exercised animals, as long as animals are submitted to a moderate-intensity training protocol. However, the neuroprotective potential of exercise is still questionable. To gain further insight into the cellular basis of the exer
Blackwell Science Inc.
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16. Reduced U snRNP assembly causes motor axon degeneration in an animal model for spinal muscular atrophy
Spinal muscular atrophy (SMA) is a motoneuron disease caused by reduced levels of survival motoneuron (SMN) protein. Previous studies have assigned SMN to uridine-rich small nuclear ribonucleoprotein particle (U snRNP) assembly, splicing, transcription, and RNA localization. Here, we have used gene silencing to assess the effect of SMN protein deficiency on
Cold Spring Harbor Laboratory Press.
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17. Cytotoxicity of immunoglobulins from amyotrophic lateral sclerosis patients on a hybrid motoneuron cell line.
Patients with amyotrophic lateral sclerosis possess antibodies (ALS IgGs) that bind to L-type skeletal muscle voltage-gated calcium channels (VGCCs) and inhibit L-type calcium current. To determine whether interaction of ALS IgGs with neuronal VGCCs might influence motoneuron survival, we used a motoneuron-neuroblastoma hybrid (VSC 4.1) cell line expressing
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18. Rescue of adult mouse motoneurons from injury-induced cell death by glial cell line-derived neurotrophic factor.
Glial cell line-derived neurotrophic factor (GDNF) has been shown to rescue developing motoneurons in vivo and in vitro from both naturally occurring and axotomy-induced cell death. To test whether GDNF has trophic effects on adult motoneurons, we used a mouse model of injury-induced adult motoneuron degeneration. Injuring adult motoneuron axons at the exit
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19. Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity.
Calbindin-D28K and/or parvalbumin appear to influence the selective vulnerability of motoneurons in amyotrophic lateral sclerosis (ALS). Their immunoreactivity is undetectable in motoneurons readily damaged in human ALS, and in differentiated motoneuron hybrid cells [ventral spinal cord (VSC 4.1 cells)] that undergo calcium-dependent apoptotic cell death in
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20. Quantitative studies on the maturation of central and peripheral parts of individual ventral motoneuron axons. II. Internodal length.
The lengths of internodes on peripheral and central stretches of the same ventral motoneuron axons were measured in 6 day rats. The former were more than twice as long as the latter. The distribution of peripheral internodal lengths was broader, and was shifted to the right, relative to that of central internodes. Short internodes were present centrally and
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21. Isolated lower motoneuron involvement following radiotherapy.
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22. Origins of Abnormal Excitability in Biceps Brachii Motoneurons of Spastic-Paretic Stroke Survivors
Stroke survivors often exhibit abnormal motoneuron excitability, manifested clinically as spasticity with exaggerated stretch reflexes in resting muscles. We examined whether this abnormal excitability is a result of increased activation of intrinsic voltage-dependent persistent inward currents (PICs) or whether it is a result of enhanced synaptic inputs to
American Physiological Society.
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23. Axonal growth of embryonic stem cell-derived motoneurons in vitro and in motoneuron-injured adult rats
We generated spinal motoneurons from embryonic stem (ES) cells to determine the developmental potential of these cells in vitro and their capacity to replace motoneurons in the adult mammalian spinal cord. ES cell-derived motoneurons extended long axons, formed neuromuscular junctions, and induced muscle contraction when cocultured with myoblasts. We transpl
National Academy of Sciences.
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24. Foxo3a induces motoneuron death through the Fas pathway in cooperation with JNK
BioMed Central.