Literatura académica sobre el tema "Motoneurones"
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Artículos de revistas sobre el tema "Motoneurones"
Büschges, A., J. Schmitz y U. Bässler. "Rhythmic patterns in the thoracic nerve cord of the stick insect induced by pilocarpine". Journal of Experimental Biology 198, n.º 2 (1 de febrero de 1995): 435–56. http://dx.doi.org/10.1242/jeb.198.2.435.
Texto completoVrbova, G., R. Navarrete y M. Lowrie. "Matching of muscle properties and motoneurone firing patterns during early stages of development". Journal of Experimental Biology 115, n.º 1 (1 de marzo de 1985): 113–23. http://dx.doi.org/10.1242/jeb.115.1.113.
Texto completoKittmann, R. "Neural mechanisms of adaptive gain control in a joint control loop: muscle force and motoneuronal activity". Journal of Experimental Biology 200, n.º 9 (1 de enero de 1997): 1383–402. http://dx.doi.org/10.1242/jeb.200.9.1383.
Texto completoCOOKE, IAN R. C. "Further Studies of Crayfish Escape Behaviour: II. Giant Axon-Mediated Neural Activity in the Appendages". Journal of Experimental Biology 118, n.º 1 (1 de septiembre de 1985): 367–77. http://dx.doi.org/10.1242/jeb.118.1.367.
Texto completoGardiner, Phillip, Eric Beaumont y Bruno Cormery. "Motoneurones "Learn" and "Forget" Physical Activity". Canadian Journal of Applied Physiology 30, n.º 3 (1 de junio de 2005): 352–70. http://dx.doi.org/10.1139/h05-127.
Texto completoNeuman, R. S. "Action of serotonin and norepinephrine on spinal motoneurones following blockade of synaptic transmission". Canadian Journal of Physiology and Pharmacology 63, n.º 6 (1 de junio de 1985): 735–38. http://dx.doi.org/10.1139/y85-120.
Texto completoRussell, D. F. "Neural basis of teeth coordination during gastric mill rhythms in spiny lobsters, Panulirus interruptus". Journal of Experimental Biology 114, n.º 1 (1 de enero de 1985): 99–119. http://dx.doi.org/10.1242/jeb.114.1.99.
Texto completoSears, T. A. "Structural changes in intercostal motoneurones following axotomy". Journal of Experimental Biology 132, n.º 1 (1 de septiembre de 1987): 93–109. http://dx.doi.org/10.1242/jeb.132.1.93.
Texto completoFerguson, G. P. y P. R. Benjamin. "The whole-body withdrawal response of Lymnaea stagnalis. II. Activation of central motoneurones and muscles by sensory input". Journal of Experimental Biology 158, n.º 1 (1 de julio de 1991): 97–116. http://dx.doi.org/10.1242/jeb.158.1.97.
Texto completoMurayama, M. y M. Takahata. "Neuronal mechanisms underlying the facilitatory control of uropod steering behaviour during treadmill walking in crayfish. I. Antagonistically regulated background excitability of uropod motoneurones". Journal of Experimental Biology 201, n.º 9 (1 de mayo de 1998): 1283–94. http://dx.doi.org/10.1242/jeb.201.9.1283.
Texto completoTesis sobre el tema "Motoneurones"
Fuente, Ruiz Sandra de la. "Development of new therapeutic strategies for Spinal Muscular Atrophy". Doctoral thesis, Universitat de Lleida, 2020. http://hdl.handle.net/10803/669753.
Texto completoLa atrofia muscular espinal (AME) es una enfermedad neurodegenerativa grave y la primera causa genética de muerte infantil. Se origina por la pérdida o mutación del gen Survival Motor Neuron 1 (SMN1) que causa una deficiencia de la proteína de Survival Motor Neuron (SMN). La reducción de esta proteína conduce predominantemente a la degeneración de las motoneuronas (MNs) de la médula espinal y, en consecuencia, produce atrofia y debilidad del músculo esquelético. Actualmente, solo se conoce parcialmente que mecanismos celulares y moleculares exactos son los responsables de la pérdida de función de las MNs. La reducción de SMN causa degeneración de neuritas y muerte celular sin características apoptóticas clásicas. La autofagia es un proceso importante y altamente regulado, esencial para la eliminación de orgánulos dañados y sustancias o proteínas tóxicas a través de la degradación con los lisosomas. La autofagia es especialmente importante en células post-mitóticas, como las MNs, donde la acumulación de autofagosomas provoca la interrupción del transporte axonal, la interferencia del tráfico intracelular y la degeneración de las neuritas. Lo que es bien sabido en la AME es que el nivel intracelular de proteína SMN define el inicio y la gravedad de la enfermedad y esto está parcialmente determinado por el número de copias del gen SMN2, la duplicación centromérica de SMN y el principal modificador de la AME. Por esa razón, comprender los procesos que regulan la degradación de SMN con la finalidad de identificar compuestos que aumentan los niveles de proteínas es el principal objetivo en el desarrollo terapéutico de AME. Las calpaínas son una familia de proteasas dependientes de calcio que se han relacionado con trastornos musculares y enfermedades neurodegenerativas. Específicamente, se ha descrito en el músculo que SMN puede ser proteolizada por calpaína. La actividad de la calpaína también está involucrada en la regulación de la autofagia mediante la modulación de múltiples de las proteínas involucradas en el proceso. El objetivo en el presente trabajo ha sido analizar la desregulación de la autofagia y determinar la participación de la calpaína en la regulación de la proteína SMN en las MNs para profundizar en el origen de la neurodegeneración y desarrollar un nuevo enfoque terapéutico para la AME. Con este fin, hemos analizado marcadores autofágicos en diferentes modelos in vitro de AME, tanto de ratón como de humano. Los resultados mostraron que los autofagosomas y los niveles de LC3 se encuentran aumentados en las muestras de AME en comparación con los controles, lo que sugiere una desregulación del proceso de autofagia a lo largo de la progresión de la enfermedad. Además, la reducción de los niveles endógenos de calpaína utilizando un shRNA muestraron un aumento de los niveles de Smn y LC3, a la vez que previene la degeneración neuritica que se produce en las MNs de ratón afectados por AME. Se obtuvieron resultados similares en experimentos in vitro utilizando un inhibidor farmacológico de calpaína, la calpeptina. Asimismo, la activación de calpaína producida por condiciones despolarizantes inducia la proteólisis de α-fodrina y de SMN, lo que confirma que calpain regula directamente los niveles de proteína SMN en las MNs. Además, el tratamiento con calpeptina in vivo mejoró significativamente la esperanza de vida y la función motora de dos modelos de ratones con AME, lo que demuestra la utilidad potencial de los inhibidores de la calpaína en la terapia para la enfermedad. Finalmente, el análisis de la vía de la calpaína en ratones y modelos celulares humanos de AME indicó un aumento de la actividad de la calpaína en las MNs con niveles reducidos de SMN. Por lo tanto, nuestros resultados demuestran que la actividad de la calpaína se encuentra sobreactivada en las MNs de AME y su inhibición puede tener un efecto beneficioso sobre el fenotipo de la enfermedad a través del aumento de SMN y la regulación del proceso de autofagia en las MNs de la médula espinal.
Spinal Muscular Atrophy (SMA) is a severe neurodegenerative disease and the first genetic cause of infant death. It is originated by the deletion or mutation of Survival Motor Neuron 1 (SMN1) gene causing a Survival Motor Neuron (SMN) protein deficiency. The reduction of this protein predominantly leads to the degeneration of spinal cord motoneurons (MNs) and consequently produces skeletal muscle atrophy and weakness. The exact cellular and molecular mechanisms responsible for MN loss of function are only partially known. SMN reduction causes neurite degeneration and cell death without classical apoptotic features. Autophagy is an important and highly regulated process, essential for the removal of damaged organelles and toxic substances or proteins through lysosome degradation. This mechanism is specifically important in post-mitotic cells like MNs where autophagosome accumulation causes axonal transport disruption, interference of intracellular space trafficking, and neurite degeneration. What is well known in SMA is that intracellular SMN protein levels are critical to define the disease onset and severity, and this is partially determined by the number of copies of SMN2, the centromeric duplication of the SMN gene and the main modifier of SMA. For that reason, understanding the processes of SMN stability and degradation to identify compounds that increase protein levels is a major goal in SMA therapeutics development. Calpains are a family of calcium-dependent proteases that have been related to muscle disorders and neurodegenerative diseases. Specifically, it has been described in muscle that SMN can be a proteolytic target of calpain. Calpain activity is also involved in autophagy regulation by modulation of multiple proteins involved in the process. The objectives in the present work have been to analyze the autophagy deregulation and determine the involvement of calpain in SMN protein regulation on MNs, in order to deepen in the origin of neurodegeneration and to develop a new therapeutic approach for SMA disease. To this end, we have analyzed autophagic markers in different mouse and human SMA in vitro models. The results showed that autophagosomes and LC3 levels were increased in SMA samples compared to controls, suggesting a deregulation of the autophagy process throughout the disease progression. Moreover, calpain knockdown using an shRNA approach showed an increase of both, Smn and LC3 levels and prevented neurite degeneration occurred in SMA affected mouse MNs. Similar results were obtained in in vitro experiments using a pharmacological calpain inhibitor, calpeptin. Likewise, calpain activation produced by depolarized conditions induced α-fodrin and SMN proteolysis, confirming that calpain directly regulates the SMN protein level in MNs. Additionally, calpeptin in vivo treatment significantly improved the lifespan and motor function of two severe SMA mouse models, demonstrating the potential utility of calpain inhibitors in SMA therapeutics. Finally, the analysis of calpain pathway members in mice and human cellular SMA models indicated an increase of calpain activity in SMN-reduced MNs. Thus, our results show that calpain activity is increased in SMA MNs and its inhibition may have a beneficial effect on the SMA phenotype through the increase of SMN and the regulation of the autophagy process in spinal cord MNs.
Sedel, Frédéric. "Mécanisme de programmation de la mort des motoneurones embryonnaires". Paris 6, 2005. http://www.theses.fr/2005PA066611.
Texto completoSahal, Anil. "The monoaminergic control of gamma motoneurones". Thesis, University of Glasgow, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394767.
Texto completoLeroy, Félix. "Atteinte différentielle de deux populations de motoneurones spinaux chez le souriceau SOD1 G93A (modèle de la maladie de Charcot)". Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T063/document.
Texto completoIn the second postnatal week, the locomotor behavior of mice changes from crawling to walking. This is made possible by profound changes in motor units. Yet, how the discharge properties of spinal motoneurons evolve during post-‐natal maturation and whether they have an effect on the motor unit maturation remains an open question. In neonates, the spinal motoneurons display two modes of discharge. For threshold pulses, 33% of the motoneurons have a discharge that start at the current onset and adapts during the pulse (“immediate firing motoneurons”). The remaining 66% motoneurons fire with a large delay and the discharge then accelerates throughout the pulse (“delayed firing motoneurons”). Though the delayed firing pattern is quite common in spinal motoneurons of neonates, the ionic mechanisms that elicit this mode of discharge have received little attention. Using the patch-clamp technique to record P6‐P10 mouse motoneurons in a spinal cord slice preparation, I characterized the ionic currents that underlie the delayed firing pattern. This is caused by a combination of an A-like potassium current that acts on a short time scale and a slow‐inactivating potassium current that delays the discharge on a much longer time scale. I then investigated how these two potassium currents contribute to the recruitment threshold and how they shape the F-I function of delayed motoneurons in neonatal mice. The slow inactivating potassium current induces memory effects that have a strong impact on motoneuron excitability and on its discharge. Building on these results, I tried to correlate the discharge pattern to known physiological sub‐types. The delayed firing motoneurons have a larger input conductance, a higher rheobase, a narrower action potential, a shorter AHP and a more complex dendritic arbor than the immediate firing motoneurons. Additionally, only a sub-‐population of the delayed firing motoneurons expressed the chondrolectin protein, a fast motoneuron marker. Based on this body of corroborating evidence, the immediate firing motoneurons would be slow type motoneurons whereas the delayed firing motoneurons would be fast type motoneurons. Finally, numerous electrical and geometrical abnormalities have been observed in spinal motoneurons of SOD1 G934 mice (model of the amyotrophic lateral sclerosis) during the second post-natal week but the results were somehow contradictory. In relation to the known differential sensitivity to the disease exhibited by slow and fast motoneurons, I investigated whether the immediate and delayed firing motoneurons are equally affected by the SOD1 mutation. This is not the case. I found that the SOD1 mutation induced a decrease in the rheobase and a hyperpolarization of the voltage threshold only in the immediate firing motoneurons, thereby making them more excitable than in WT mice. Furthermore, the dendrites of the immediate firing motoneurons are substantially shorter (about 35%) in the mutant than in the WT. In sharp contrast, the excitability of the delayed firing motoneurons is unchanged and the dendritic tree is nearly unaffected (the dendrites only undergo a 10% elongation). These results allow for reconsidering the link between hyperexcitability and degenerescence of the motoneurons
Teixidó, Viyuela Laura. "Factors sèrics en l’Esclerosi Lateral Amiotròfica. Modulació del receptor de glutamat de tipus NMDA GluN1/GluN2A". Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/79039.
Texto completoAmyotrophic lateral sclerosis (ALS) is a devastating neuromuscular disease, characterized by the selective degeneration of the superior motor neurons in the motor cortex and of the inferior motor neurons in the brain-stem and spinal cord. The familial form of the illness is associated with the mutation of the superoxide dismutase enzyme (SOD-1). This and other mutations accounts for fewer than 10% of cases; the rest, more than 90%, correspond to the sporadic form. In this study we tested the effect of sera from sporadic ALS patients and from mutated human SOD-1 (mSOD1 G93A) transgenic rats on N-methyl-D-aspartate receptors (NMDAR). We hypothesize that an endogenous excitotoxic factor is implicated in neuronal death in ALS, mediated by the activation of NMDAR noncanonical signalling pathways. Sera from ALS patients or healthy subjects were pretreated to inactivate complement pathways and dialysed to remove glutamate. Sera from mSOD1 G93A rats were obtained at different stages of the neurodegenerative progression. Sera from transgenic rats were also pretreated to eliminate complement system and glutamate. Immunoglobulins G (IgGs) from ALS patients and healthy subjects were obtained by affinity chromatography and dialyzed against phosphate-buffered saline. Human NMDAR were expressed in Xenopus laevis oocytes, and glutamate-induced currents were recorded using the two electrode voltage clamp technique. We observed that sera from sporadic ALS patients induced transient oscillatory currents in Xenopus oocytes expressing NMDAR with a total electric charge significantly higher than the electric charge carried by currents induced by sera from healthy subjects. The currents were inhibited by MK-801, a noncompetitive blocker of NMDAR. Results of sera from mSOD1 G93A transgenic rats were similar to those of sera from ALS patients; samples from patients with another type of neuromuscular disease did not exert this effect. IgG from ALS patients have a significant effect on NMDAR-injected oocytes and that response was doubled respect to the observed in the case of IgG from healthy subjects. Our data agree with the view that ALS patients sera contain some soluble factors that activates NMDAR, not opening directly the ionic conductance, but activating a non-canonical pathway.
Bouhadfane, Mouloud. "Propriétés électriques bistables des motoneurones de la moelle épinière : Identification des mécanismes ioniques sous-jacents". Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5030/document.
Texto completoPosture allowing an erect posture of the body relies on spiking activity of motoneurons innervating antigravitary muscle. Discharge could take the form of plateau potential on mature motoneurons of numerous vertebrates. To determine a possible concordance between the emergence of plateau potential and postural control development, we studied the maturation and ionic nature of plateau potential of motoneurons innervating triceps surae muscle of neonatal rat.The conclusion of our work allows us to propose a fundamental mechanism in the genesis of plateau potential on lumbar motoneurons. This mechanism based on a "ménage a trois" seems to play an important role in the neonatal motor development. This scientific advance could eventually lead to a better understanding of the origin of some sensori-motor impairments (spasticity, hyperalgesia...) and development of therapeutic strategies
SIMON, MAGDA. "Developpement postnatal des motoneurones spinaux lombaires du chat : identification des motoneurones alpha et gamma et remaniements de leur equipement synaptique". Paris 6, 1996. http://www.theses.fr/1996PA066391.
Texto completoAllard, Ludivine. "Dysfonctions mitochondriales et homéostasie bioénergétique des motoneurones dans un modèle de sclérose latérale amyotrophique". Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22088/document.
Texto completoAmyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disorder characterized by a loss of motor neurons, leading to muscle wasting and weakness. Mutations in superoxide dismutase-1 (SOD1) cause a form of ALS. As in ALS patients, the mutant SOD1 animal model of ALS reveals that not all motor neurons are equally susceptible to the disease process. An attractive mechanism underlying differential susceptibility is the variable bioenergetics need of distinct subsets of motor neurons. This implies that within the CNS, bioenergetics can modulate the pathological threshold. Even in the absence of loss in bioenergetics, one can envision a situation in which a pathological stress alters the level at which either the production or delivery of ATP becomes insufficient, precipitating the demise of the most vulnerable neuron types. In neurons, majority of ATP is produced by mitochondria and the homeostasis of ion gradients is the most energy-consuming process. Reduced mitochondrial function will modify the electrical properties of motor neurons if ATP availability becomes insufficient to allow ion pumps to maintain appropriate gradients. We demonstrated that the basal ATP intra-cellular concentration in motor neuron cultures lower in SOD1 mutated cells compared to wild type. Paradoxically to this result, the oxygen consumption rate of mitochondria is increase in mSOD1 cells and there is no evidence for an increase of consumption. Our results support the interesting hypothesis that there is an uncoupling between the respiratory chain and the ATP production. This uncoupling might be used as a strategy to minor the toxic properties of hyper stimulated mitochondrion
Conway, Elizabeth Ann. "The development of corticospinal projections in man". Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296148.
Texto completoEvans, Pamela. "Crossed reflexes of the human lower limbs : a study using the Hoffman reflex". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367596.
Texto completoLibros sobre el tema "Motoneurones"
O'Donovan, Michael J. y Mélanie Falgairolle, eds. Vertebrate Motoneurons. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07167-6.
Texto completoImaharu, Nakano y Hirano Asao 1926-, eds. Amyotrophic lateral sclerosis: Progress and perspectives in basic research and clinical application : proceedings of the 11th Tokyo Metropolitan Institute for Neuroscience (TMIN) International Symposium, Tokyo, October 25-27, 1995. Amsterdam: Elsevier Science, 1996.
Buscar texto completoA, Wernig, ed. Plasticity of motoneuronal connections. Amsterdam: Elsevier, 1991.
Buscar texto completoStewart, Bryan A. Synaptic plasticity in a regenerated crayfish phasic motoneuron. Ottawa: National Library of Canada, 1992.
Buscar texto completoKrammer, Eva B., Martin F. Lischka, Thomas P. Egger, Maria Riedl y Helmut Gruber. The Motoneuronal Organization of the Spinal Accessory Nuclear Complex. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-662-10362-3.
Texto completo1944-, Krammer E. B., ed. The Motoneuronal organization of the spinal accessory nuclear complex. Berlin: Springer-Verlag, 1987.
Buscar texto completoOrth, Peter M. R. Phosphorylation-dependent plasticity at synapses of a crayfish phasic motoneuron. Ottawa: National Library of Canada, 2002.
Buscar texto completoPatel, Varsha. Neuromuscular synaptic differentiation of a crab motoneuron in four separate muscles. Ottawa: National Library of Canada, 1996.
Buscar texto completoHirji, Rahim. Structure of regenerated synaptic connections of allotransplanted phasic motoneurons on a tonic muscle in crayfish. Ottawa: National Library of Canada, 1999.
Buscar texto completoCampbell, Jessica J. An investigation into factors affecting motoneuron regeneration in the rat sciatic nerve. Ottawa: National Library of Canada, 1990.
Buscar texto completoCapítulos de libros sobre el tema "Motoneurones"
Brock, L. G., J. S. Coombs y J. C. Eccles. "Antidromic Propagation of Impulses into Motoneurones". En Ciba Foundation Symposium - The Spinal Cord, 120–31. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718827.ch11.
Texto completoMendell, Lorne M. "Synaptic Differentiation on Type Identified Motoneurones". En Alpha and Gamma Motor Systems, 3–8. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1935-5_1.
Texto completoAlaburda, Aidas, Jean-François Perrier y Jørn Hounsgaard. "Mechanisms Causing Plateau Potentials in Spinal Motoneurones". En Advances in Experimental Medicine and Biology, 219–26. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0713-0_27.
Texto completoKutsch, W. y R. Heckmann. "Homologous structures, exemplified by motoneurones of Mandibulata". En Experientia Supplementum, 221–48. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-9219-3_11.
Texto completoAwiszus, Friedemann y Helmut Feistner. "The “Size Principle” of Human α-Motoneurones". En Alpha and Gamma Motor Systems, 65–70. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1935-5_14.
Texto completoCollins, David F., Monica Gorassini, David Bennett, David Burke y Simon C. Gandevia. "Recent Evidence for Plateau Potentials in Human Motoneurones". En Advances in Experimental Medicine and Biology, 227–35. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0713-0_28.
Texto completoJohnson, I. P., Y. S. Simaika y T. A. Sears. "Synaptic Loss from Axotomised α- and γ-Motoneurones". En Alpha and Gamma Motor Systems, 51–53. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1935-5_10.
Texto completoSkorupski, P. "Central and Reflex Recruitment of Crayfish Leg Motoneurones". En Neural Control of Movement, 261–68. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1985-0_32.
Texto completoSears, T. A., I. P. Johnson y A. H. Pullen. "Ultrastructural Analysis of Target-Dependent Properties of Mammalian Motoneurones". En Advances in Applied Neurological Sciences, 143–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71540-2_16.
Texto completoKernell, Daniel. "Things We Know and Do Not Know About Motoneurones". En Advances in Experimental Medicine and Biology, 187–92. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0713-0_22.
Texto completoActas de conferencias sobre el tema "Motoneurones"
Leão, Arthur Ventura Martins, Alexandre Leite Rodrigues de Oliveira y Luciana Politti Cartarozzi. "Neuroprotection by memantine after compressive spinal root lesion". En XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.383.
Texto completoSerradori, Massimiliano, Marco Gherardi, Luciano Gabbrielli, Claudio Bettini, Ferruccio Aquilini, Giovanni D'Ambrosio, Antonio Servino y Alessandro Celi. "Prognostic determinants in motoneuron diseases". En ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1907.
Texto completoShapiro, Nicholas P. y Robert H. Lee. "Synaptic Amplification in Motoneurons: Computational and Mechanistic Implications". En Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260838.
Texto completoShapiro, Nicholas P. y Robert H. Lee. "Synaptic Amplification in Motoneurons: Computational and Mechanistic Implications". En Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397474.
Texto completoGamal, Mai, Mohamed H. Mousa, Seif Eldawlatly y Sherif M. Elbasiouny. "Automated Cell-Type Classification and Death-Detection of Spinal Motoneurons". En 2018 9th Cairo International Biomedical Engineering Conference (CIBEC). IEEE, 2018. http://dx.doi.org/10.1109/cibec.2018.8641824.
Texto completoChmykhova, Nadezhda, Natalia Kalinina, Aleksey Zaitsev y Nikolai Vesselkin. "MODULATION OF LUMBAR MOTONEURONS ACTIVITY BY METABOTROPIC GLUTAMATE AND SEROTONIN RECEPTORS". En XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m620.sudak.ns2019-15/457.
Texto completoYao Li, L. H. Smith, L. J. Hargrove, D. J. Weber y G. E. Loeb. "Estimation of excitatory drive from sparse motoneuron sampling". En 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346752.
Texto completoMousa, Mohamed H., Ahmed H. Kandil y Sherif M. Elbasiouny. "Simulation of dendritic L-type ca channels' warm-up phenomenon in spinal motoneurons". En 2016 8th Cairo International Biomedical Engineering Conference (CIBEC). IEEE, 2016. http://dx.doi.org/10.1109/cibec.2016.7836113.
Texto completoSuresh, A. K., Xiaogang Hu, R. K. Powers y W. Z. Rymer. "Examination of afterhyperpolarization duration changes in motoneurons innervating paretic muscles in stroke survivors". En 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346740.
Texto completoCisi, Rogerio R. L. y Andre F. Kohn. "H-reflex depression simulated by a biologically realistic motoneuron network". En 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352889.
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