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Thematische Bibliographien / Motorneurone / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Motorneurone“

Autor: Grafiati

Veröffentlicht am 16. November 2024

Zuletzt aktualisiert am 31. Juli 2025

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1

Braak, H., M. Neumann, A. Ludolph, and K. Del Tredici. "Breitet sich die sporadisch auftretende amyotrophe Lateralsklerose über axonale Verbindungen aus?" Aktuelle Neurologie 44, no. 06 (2017): 409–14. http://dx.doi.org/10.1055/s-0043-111405.

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ZusammenfassungDer pathologische Prozess einer sporadisch auftretenden amyotrophen Lateralsklerose (sALS) ist mit dem Auftreten zytoplasmatischer Einschlusskörper eines normalerweise im Zellkern vorkommenden Proteins (TDP-43) verbunden und ergreift nur wenige Arten langaxoniger Projektionsneurone. Die Riesenpyramidenzellen von Betz im primären motorischen Neokortex und die α-Motorneurone im unteren Hirnstamm und Rückenmark sind früh ergriffene Zellformen. Im zentralen Nervensystem des Menschen sind diese beiden Zellarten durch axonale Projektionen monosynaptisch verbunden. Im Verlauf einer sAL

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2

GUILOFF, R. J. "Use of TRH Analogues in Motorneurone Disease." Annals of the New York Academy of Sciences 553, no. 1 Thyrotropin-R (1989): 399–421. http://dx.doi.org/10.1111/j.1749-6632.1989.tb46662.x.

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3

Pall, HardevS, AdrianC Williams, Rosemary Waring, and Elwyn Elias. "MOTORNEURONE DISEASE AS MANIFESTATION OF PESTICIDE TOXICITY." Lancet 330, no. 8560 (1987): 685. http://dx.doi.org/10.1016/s0140-6736(87)92468-8.

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4

Jacobs, K., M. G. Todman, M. J. Allen, J. A. Davies, and J. P. Bacon. "Synaptogenesis in the giant-fibre system of Drosophila: interaction of the giant fibre and its major motorneuronal target." Development 127, no. 23 (2000): 5203–12. http://dx.doi.org/10.1242/dev.127.23.5203.

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The tergotrochanteral (jump) motorneuron is a major synaptic target of the Giant Fibre in Drosophila. These two neurons are major components of the fly's Giant-Fibre escape system. Our previous work has described the development of the Giant Fibre in early metamorphosis and the involvement of the shaking-B locus in the formation of its electrical synapses. In the present study, we have investigated the development of the tergotrochanteral motorneuron and its electrical synapses by transforming Drosophila with a Gal4 fusion construct containing sequences largely upstream of, but including, the

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Mills, K. "Update on ALS: assessing the upper motorneurone component." Clinical Neurophysiology 119 (May 2008): S8. http://dx.doi.org/10.1016/s1388-2457(08)60035-8.

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Leigh, P. N. "DS1.1 Motorneurone degeneration: ALS and its clinical variants." Clinical Neurophysiology 117 (September 2006): 1. http://dx.doi.org/10.1016/j.clinph.2006.07.049.

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7

Tissenbaum, H. A., and D. J. Parry. "The effect of partial denervation of tibialis anterior (TA) muscle on the number and sizes of motorneurons in TA motornucleus of normal and dystrophic (C57BL dy2j/dy2j) mice." Canadian Journal of Physiology and Pharmacology 69, no. 11 (1991): 1769–73. http://dx.doi.org/10.1139/y91-261.

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The tibialis anterior (TA) muscle in one leg of normal (C57BL) and dystrophic (dy2j) mice was partially denervated by resection of a part of the lateral popliteal nerve. Two months later the muscle was injected with horseradish peroxidase to permit visualization of the motorneurons that survived. Partial denervation in both C57 and dy2j mice resulted in reduction of the number of motorneurons that supplied the muscle to approximately one-half the normal complement. The surviving motorneurons were found to be significantly larger (about 25%) than their contralateral counterparts. This condition

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Abbott, R. J., D. Holder, and S. Currie. "FALSE POSITIVE ANTI ACETYLCHOLINE RECEPTOR ANTIBODIES IN MOTORNEURONE DISEASE." Lancet 327, no. 8486 (1986): 906–7. http://dx.doi.org/10.1016/s0140-6736(86)91005-6.

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9

Ashizawa, T. "FALSE POSITIVE ANTI-ACETYLCHOLINE RECEPTOR ANTIBODIES IN MOTORNEURONE DISEASE." Lancet 327, no. 8492 (1986): 1272. http://dx.doi.org/10.1016/s0140-6736(86)91408-x.

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10

Spencer, PeterS, PeterB Nunn, Jacques Hugon, Albert Ludolph, and DwijendraN Roy. "MOTORNEURONE DISEASE ON GUAM: POSSIBLE ROLE OF A FOOD NEUROTOXIN." Lancet 327, no. 8487 (1986): 965. http://dx.doi.org/10.1016/s0140-6736(86)91059-7.

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11

Chang, S., J. Fan, and J. Nayak. "Pathfinding by cranial nerve VII (facial) motorneurons in the chick hindbrain." Development 114, no. 3 (1992): 815–23. http://dx.doi.org/10.1242/dev.114.3.815.

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Cranial nerve VII (facial) motorneurons begin extending axons through rhombomeres 4 and 5 (R4 and R5) in the chick hindbrain on the second day of incubation. Without crossing the midline, facial motorneuron axons extend laterally from a ventromedial cell body location. All facial motorneuron axons leave the hindbrain through a discrete exit site in R4. To examine the importance of the exit site in R4 on motorneuron pathfinding, we ablated R4 before motorneuron axonogenesis. We find that mechanisms intrinsic to R5 direct the initial lateral orientation of R5 motorneuron axons. Upon reaching a p

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12

Segerberg, M. A., and A. O. Stretton. "Actions of cholinergic drugs in the nematode Ascaris suum. Complex pharmacology of muscle and motorneurons." Journal of General Physiology 101, no. 2 (1993): 271–96. http://dx.doi.org/10.1085/jgp.101.2.271.

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The cholinergic agonists acetylcholine (ACh), nicotine, and pilocarpine produced depolarizations and contractions of muscle of the nematode Ascaris suum. Dose-dependent depolarization and contraction by ACh were suppressed by about two orders of magnitude by 100 microM d-tubocurarine (dTC), a nicotinic antagonist, but only about fivefold by 100 microM N-methyl-scopolamine (NMS), a muscarinic antagonist. NMS itself depolarized both normal and synaptically isolated muscle cells. The muscle depolarizing action of pilocarpine was not consistently antagonized by either NMS or dTC. ACh receptors wer

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SATTERLIE, RICHARD A., and ANDREW N. SPENCER. "Swimming in the Pteropod Mollusc, Clione Limacina: II. Physiology." Journal of Experimental Biology 116, no. 1 (1985): 205–22. http://dx.doi.org/10.1242/jeb.116.1.205.

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The central pattern generator (CPG) for swimming inClione limacina was localized in cutting experiments. A separate pattern generator for each wing islocated in the ipsilateral pedal ganglion. The CPGs are tightly coupled butcan be isolated by severing the pedal commissure. Removal of the cerebralganglia results in a decrease in swim frequency and regularity suggesting descending modulation of the CPGs. Two classes of pedal neurones display firing patterns in phase with swimming movements. One class, swim motor neurones, are further divided intodepressor and elevator groups. Motor neurone reco

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Maitland, D. P., and W. J. Heitler. "A Motorneurone Cell Body Located Either Dorsally or Ventrally within a Crustacean Abdominal Ganglion." Acta Zoologica 68, no. 1 (1987): 9–16. http://dx.doi.org/10.1111/j.1463-6395.1987.tb00872.x.

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15

Modarres-Sadeghi, H., and R. J. Guiloff. "Subacute Administration of A TRH Analogue (RX77368) to Patients with Motorneurone Disease (MND) Pilot Study." Clinical Science 72, s16 (1987): 48P. http://dx.doi.org/10.1042/cs072048pa.

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16

Khan, J. K., Y. H. Kuo, A. Haque, and F. Lambein. "Inhibitory and excitatory amino acids in cerebrospinal fluid of neurolathyrism patients, a highly prevalent motorneurone disease." Acta Neurologica Scandinavica 91, no. 6 (2009): 506–10. http://dx.doi.org/10.1111/j.1600-0404.1995.tb00454.x.

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17

Bascal, Z. A., A. Montgomery, L. Holden-Dye, R. G. Williams, and R. J. Walker. "Histochemical mapping of NADPH diaphorase in the nervous system of the parasitic nematode Ascaris suum." Parasitology 110, no. 5 (1995): 625–37. http://dx.doi.org/10.1017/s0031182000065343.

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SUMMARYNADPH diaphorase has recently been discovered to be responsible for neuronal nitric oxide (NO) synthase activity in mammals. It thus serves as a histochemical marker for the localization of NO synthase in the nervous system. The histochemical technique was used to map out potential NO-producing neurones in the nervous system of the parasitic nematode, Ascaris suum. Positive staining for NADPH diaphorase was present in various parts of the central nervous system, in particular within selective cell bodies and fibres in the ventral ganglion, the retrovesicular ganglion, ventral and dorsal

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18

Shreffler, W., T. Magardino, K. Shekdar, and E. Wolinsky. "The unc-8 and sup-40 genes regulate ion channel function in Caenorhabditis elegans motorneurons." Genetics 139, no. 3 (1995): 1261–72. http://dx.doi.org/10.1093/genetics/139.3.1261.

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Abstract Two Caenorhabditis elegans genes, unc-8 and sup-40, have been newly identified, by genetic criteria, as regulating ion channel function in motorneurons. Two dominant unc-8 alleles cause motorneuron swelling similar to that of other neuronal types in dominant mutants of the deg-1 gene family, which is homologous to a mammalian gene family encoding amiloride-sensitive sodium channel subunits. As for previously identified deg-1 family members, unc-8 dominant mutations are recessively suppressed by mutations in the mec-6 gene, which probably encodes a second type of channel component. An

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Ciriza, Jesús, Marcos García-Ojeda, Inmaculada Martín-Burriel, et al. "Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein." Open Life Sciences 3, no. 2 (2008): 105–12. http://dx.doi.org/10.2478/s11535-008-0011-z.

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AbstractNeurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested be

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Lambein, Fernand, Rabiul Haque, Jehangir K. Khan, Naod Kebede, and Yu-Haey Kuo. "From soil to brain: Zinc deficiency increases the neurotoxicity of Lathyrus sativus and may affect the susceptibility for the motorneurone disease neurolathyrism." Toxicon 32, no. 4 (1994): 461–66. http://dx.doi.org/10.1016/0041-0101(94)90298-4.

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21

Colomb, Julien, and Björn Brembs. "PKC in motorneurons underlies self-learning, a form of motor learning inDrosophila." PeerJ 4 (April 25, 2016): e1971. http://dx.doi.org/10.7717/peerj.1971.

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Tethering a fly for stationary flight allows for exquisite control of its sensory input, such as visual or olfactory stimuli or a punishing infrared laser beam. A torque meter measures the turning attempts of the tethered fly around its vertical body axis. By punishing, say, left turning attempts (in a homogeneous environment), one can train a fly to restrict its behaviour to right turning attempts. It was recently discovered that this form of operant conditioning (called operant self-learning), may constitute a form of motor learning inDrosophila. Previous work had shown that Protein Kinase C

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DAVIS, R. E. "Action of excitatory amino acids on hypodermis and the motornervous system of Ascaris suum: pharmacological evidence for a glutamate transporter." Parasitology 116, no. 5 (1998): 487–500. http://dx.doi.org/10.1017/s0031182098002479.

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Electrophysiological and pharmacological experiments suggest the presence of an electrogenic glutamate transporter in the motornervous system of the parasitic nematode Ascaris suum. This putative transporter occurs in hypodermis (a tissue in some respects analogous to glia) and in DE2 motorneurons, a dorsal excitatory motorneuron class which receives excitatory glutamatergic post-synaptic potentials. Glutamate application to hypodermis produced non-conductance mediated depolarizations that were smaller in amplitude and slower in rate of rise than DE2 responses where a glutamate-activated condu

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Prokop, Andreas, Jay Uhler, John Roote, and Michael Bate. "The kakapo Mutation Affects Terminal Arborization and Central Dendritic Sprouting of Drosophila Motorneurons." Journal of Cell Biology 143, no. 5 (1998): 1283–94. http://dx.doi.org/10.1083/jcb.143.5.1283.

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The lethal mutation l(2)CA4 causes specific defects in local growth of neuronal processes. We uncovered four alleles of l(2)CA4 and mapped it to bands 50A-C on the polytene chromosomes and found it to be allelic to kakapo (Prout et al. 1997. Genetics. 146:275– 285). In embryos carrying our kakapo mutant alleles, motorneurons form correct nerve branches, showing that long distance growth of neuronal processes is unaffected. However, neuromuscular junctions (NMJs) fail to form normal local arbors on their target muscles and are significantly reduced in size. In agreement with this finding, antib

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Steventon, G., R. H. Waring, A. C. Williams, H. S. Pall, and D. Adams. "XENOBIOTIC METABOLISM IN MOTORNEURON DISEASE." Lancet 332, no. 8612 (1988): 644–47. http://dx.doi.org/10.1016/s0140-6736(88)90467-9.

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Gladchenko, D. A., I. V. Alekseeva, A. A. Chelnokov, and M. G. Barkanov. "Modelling of impulse activity of afferent fibers of antagonist muscles during transcutaneous electrical stimulation of the spinal cord during walking." Физиология человека 50, no. 1 (2024): 34–44. http://dx.doi.org/10.31857/s0131164624010035.

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The article describes the results of studies on the impulse activity of various groups of afferent fibers and EMG patterns of lower leg antagonist muscles when walking without, during and after transcutaneous electrical stimulation of the dorsal roots of the lower thoracic spinal cord of a person. Using a mathematical model based on the prediction of the triggering of muscle spindles, variability in the manifestation of impulse activity of various afferents tibialis anterior muscle (TA) and gastrocnemius medialis muscle (GM) when walking under different experimental conditions is shown. It was

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Sabatier, Fabienne, Justine Chaigne, Maryse Martin, et al. "Abstract 7178: Neuronal cells derived from iPSCs cell to evaluate neurotoxicity after 48 or 72 hours in high-through put screening format." Cancer Research 84, no. 6_Supplement (2024): 7178. http://dx.doi.org/10.1158/1538-7445.am2024-7178.

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Abstract Neurotoxicity is a major concern in central nervous system drug discovery and a frequent cause of attrition in clinical trials or approved drug withdrawal. Neuropathy is a side effect defined by the injury of peripheral nerves causing a loss of sensation/motion. Drug development pipelines typically involve testing in cell lines followed by animal investigations with translation to humans. The induced pluripotent stem cells (iPSCs) have widened new model systems to study adverse toxicities. With evolution in regulatory guidance the use of human- iPSC-derived tissue provides high-throug

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Schauerte, H. E., F. J. van Eeden, C. Fricke, J. Odenthal, U. Strahle, and P. Haffter. "Sonic hedgehog is not required for the induction of medial floor plate cells in the zebrafish." Development 125, no. 15 (1998): 2983–93. http://dx.doi.org/10.1242/dev.125.15.2983.

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Sonic hedgehog (Shh) is a secreted protein that is involved in the organization and patterning of several tissues in vertebrates. We show that the zebrafish sonic-you (syu) gene, a member of a group of five genes required for somite patterning, is encoding Shh. Embryos mutant for a deletion of syu display defects in patterning of the somites, the lateral floor plate cells, the pectoral fins, the axons of motorneurons and the retinal ganglion cells. In contrast to mouse embryos lacking Shh activity, syu mutant embryos do form medial floor plate cells and motorneurons. Since ectopic overexpressi

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Walker, Sarah, Gaynor Spencer, Aleksandar Necakov, and Robert Carlone. "Identification and Characterization of microRNAs during Retinoic Acid-Induced Regeneration of a Molluscan Central Nervous System." International Journal of Molecular Sciences 19, no. 9 (2018): 2741. http://dx.doi.org/10.3390/ijms19092741.

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Retinoic acid (RA) is the biologically active metabolite of vitamin A and has become a well-established factor that induces neurite outgrowth and regeneration in both vertebrates and invertebrates. However, the underlying regulatory mechanisms that may mediate RA-induced neurite sprouting remain unclear. In the past decade, microRNAs have emerged as important regulators of nervous system development and regeneration, and have been shown to contribute to processes such as neurite sprouting. However, few studies have demonstrated the role of miRNAs in RA-induced neurite sprouting. By miRNA seque

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Kreutzberg, Georg W., Manuel B. Graeber, and Wolfgang J. Streit. "Neuron-glial relationship during regeneration of motorneurons." Metabolic Brain Disease 4, no. 1 (1989): 81–85. http://dx.doi.org/10.1007/bf00999498.

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Armakola, Maria, and Gary Ruvkun. "Regulation of Caenorhabditis elegans neuronal polarity by heterochronic genes." Proceedings of the National Academy of Sciences 116, no. 25 (2019): 12327–36. http://dx.doi.org/10.1073/pnas.1820928116.

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Many neurons display characteristic patterns of synaptic connections that are under genetic control. The Caenorhabditis elegans DA cholinergic motor neurons form synaptic connections only on their dorsal axons. We explored the genetic pathways that specify this polarity by screening for gene inactivations and mutations that disrupt this normal polarity of a DA motorneuron. A RAB-3::GFP fusion protein that is normally localized to presynaptic terminals along the dorsal axon of the DA9 motorneuron was used to screen for gene inactivations that disrupt the DA9 motorneuron polarity. This screen id

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Sau, Daniela, Paola Rusmini, Valeria Crippa, et al. "Dysregulation of axonal transport and motorneuron diseases." Biology of the Cell 103, no. 2 (2011): 87–107. http://dx.doi.org/10.1042/bc20100093.

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Sendtner, Michael, and Hans Thoenen. "Neurodegenerative Disease: Oxidative stress and motorneuron disease." Current Biology 4, no. 11 (1994): 1036–39. http://dx.doi.org/10.1016/s0960-9822(00)00237-2.

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Novak, Christine B., Brenda Ross, Susan E. Mackinnon, and Julian M. Nedzelski. "Facial Sensibility in Patients with Unilateral Facial Nerve Paresis." Otolaryngology–Head and Neck Surgery 109, no. 3 (1993): 506–13. http://dx.doi.org/10.1177/019459989310900320.

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This study evaluated facial sensibility in 29 patients with unilateral lower motorneuron facial nerve paresis using standard clinical tests of sensory evaluation used at other anatomic sites, most commonly the hand. Vibratory and cutaneous pressure thresholds and moving and static two-point discrimination were measured. Statistically significant differences were found between the affected and unaffected sides of the face, with vibration threshold, cutaneous pressure threshold, and static two-point discrimination being greater on the affected side. Vibration thresholds and two-point discriminat

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Konishi, Hiroaki, Takayoshi Torigoshi, Nobuyuki Ito, and Kenji Kumagai. "The study of labelling motorneurons with horseradish peroxidase." Orthopedics & Traumatology 36, no. 3 (1988): 1023–26. http://dx.doi.org/10.5035/nishiseisai.36.1023.

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Parkes, Tony L., Arthur J. Hilliker, and John P. Phillips. "Motorneurons, reactive oxygen, and life span in Drosophila☆." Neurobiology of Aging 20, no. 5 (1999): 531–35. http://dx.doi.org/10.1016/s0197-4580(99)00086-x.

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Atkinson, R. P., C. Williams, W. K. Engel, and C. A. Miller. "PROGRESSIVE MUSCULAR ATROPHY AUTOANTIBODIES BIND TO LOWER MOTORNEURONS." Journal of Neuropathology and Experimental Neurology 55, no. 5 (1996): 631. http://dx.doi.org/10.1097/00005072-199605000-00115.

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Waring, R. H., S. G. Sturman, M. C. G. Smith, G. B. Steventon, M. T. E. Heafield, and A. C. Williams. "S-METHYLATION IN MOTORNEURON DISEASE AND PARKINSON'S DISEASE." Lancet 334, no. 8659 (1989): 356–57. http://dx.doi.org/10.1016/s0140-6736(89)90538-2.

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Aquino-Nunez, Wendy, Zachery E. Mielko, Trae Dunn, et al. "cnd-1/NeuroD1 Functions with the Homeobox Gene ceh-5/Vax2 and Hox Gene ceh-13/labial To Specify Aspects of RME and DD Neuron Fate in Caenorhabditis elegans." G3 Genes|Genomes|Genetics 10, no. 9 (2020): 3071–85. http://dx.doi.org/10.1534/g3.120.401515.

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Abstract Identifying the mechanisms behind neuronal fate specification are key to understanding normal neural development in addition to neurodevelopmental disorders such as autism and schizophrenia. In vivo cell fate specification is difficult to study in vertebrates. However, the nematode Caenorhabditis elegans, with its invariant cell lineage and simple nervous system of 302 neurons, is an ideal organism to explore the earliest stages of neural development. We used a comparative transcriptome approach to examine the role of cnd-1/NeuroD1 in C. elegans nervous system development and function

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Hobert, O., K. Tessmar, and G. Ruvkun. "The Caenorhabditis elegans lim-6 LIM homeobox gene regulates neurite outgrowth and function of particular GABAergic neurons." Development 126, no. 7 (1999): 1547–62. http://dx.doi.org/10.1242/dev.126.7.1547.

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We describe here the functional analysis of the C. elegans LIM homeobox gene lim-6, the ortholog of the mammalian Lmx-1a and b genes that regulate limb, CNS, kidney and eye development. lim-6 is expressed in a small number of sensory-, inter- and motorneurons, in epithelial cells of the uterus and in the excretory system. Loss of lim-6 function affects late events in the differentiation of two classes of GABAergic motorneurons which control rhythmic enteric muscle contraction. lim-6 is required to specify the correct axon morphology of these neurons and also regulates expression of glutamic ac

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Ciriza, J., M. Moreno-Igoa, A. C. Calvo, et al. "A genetic fusion GDNF-C fragment of tetanus toxin prolongs survival in a symptomatic mouse ALS model." Restorative Neurology and Neuroscience 26, no. 6 (2008): 459–65. https://doi.org/10.3233/rnn-2008-00428.

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Purpose: Amyotrophic Lateral Sclerosis (ALS) is a paralyzing disorder that kills individuals within three to five years of onset without any possibility for effective treatment. One proposed therapy has been the use of neurotrophic factors to inhibit the apoptosis of motorneurones. At the present, one way to deliver neurotrophic factors after intramuscular injection to the motor neurones is through the use of adenoviral vectors. An alternative strategy is the use of the atoxic C fragment of tetanus toxin (TTC) as a neurotrophic factor carrier for motorneurones. Methods: We have produced the re

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Bulbulian, R., J. Burke, M. Kovach, and R. Ploutz-Snyder. "THE EFFECT OF HETERONOMOUS MUSCLE STRETCHING ON MOTORNEURON EXCITABILITY." Medicine & Science in Sports & Exercise 31, Supplement (1999): S136. http://dx.doi.org/10.1097/00005768-199905001-00554.

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Oku, Yoshitaka, Eugene N. Bruce, Chelliah R. Richmonds, and David W. Hudgel. "The carotid body in the motorneuron response to protriptyline." Respiration Physiology 93, no. 1 (1993): 41–49. http://dx.doi.org/10.1016/0034-5687(93)90066-j.

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Novikov, Anton, Maria Maldova, Natalia Shandybina, et al. "First Use of Non-Invasive Spinal Cord Stimulation in Motor Rehabilitation of Children with Spinal Muscular Atrophy." Life 13, no. 2 (2023): 449. http://dx.doi.org/10.3390/life13020449.

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Spinal muscular atrophy (SMA) is characterized by the degeneration of spinal alpha motorneurons. Nusinersen demonstrated good efficacy in the early disease phases. The feasibility of transcutaneous spinal cord stimulation (tSCS) in motor rehabilitation of patients with spinal cord injury has been demonstrated. We hypothesize that tSCS may activate intact and restored by nusinersen motorneurons and slow down the decline in motor activity, and may contribute to the development of motor skills in children with SMA. A case series is presented. Five children (6–13 years old) with SMA type II or III

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Aréchiga, Hugo, and Leonardo Rodríguez-Sosa. "Coupling of Environmental and Endogenous Factors in the Control of Rhythmic Behaviour in Decapod Crustaceans." Journal of the Marine Biological Association of the United Kingdom 77, no. 1 (1997): 17–29. http://dx.doi.org/10.1017/s0025315400033750.

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Behavioural patterns of crustaceans are known to vary within the 24 hour cycle and in relation to environmental signals. Light and chemical stimuli induce specific behavioural responses. Retinal and extra-retinal photoreceptors use different motor responses to illumination selectively. Light responsiveness is modulated at various levels, from the light admittance to the retina, up to the integration in higher order interneurones and motorneurones. An endogenous circadian rhythmicity contributes to the various elements of the system.

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Wang, Jijiang, Mustapha Irnaten, Priya Venkatesan, Cory Evans, Sunit Baxi, and David Mendelowitz. "Synaptic activation of hypoglossal respiratory motorneurons during inspiration in rats." Neuroscience Letters 332, no. 3 (2002): 195–99. http://dx.doi.org/10.1016/s0304-3940(02)00957-6.

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Funakoshi, Kengo, Da-Young Han, Miki Kobayashi, Masato Nakano, Yoshitoshi Atobe, and Tetsuo Kadota. "Differential Islet-1 expression among spinal motorneurons in prenatal mouse." Neuroscience Research 65 (January 2009): S155. http://dx.doi.org/10.1016/j.neures.2009.09.789.

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Tweedell, Andrew J., and Matthew S. Tenan. "motoRneuron: an open-source R toolbox for time-domain motor unit analyses." PeerJ 7 (December 10, 2019): e7907. http://dx.doi.org/10.7717/peerj.7907.

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Motor unit synchronization is the tendency of motor neurons and their associated muscle fibers to discharge near-simultaneously. It has been theorized as a control mechanism for force generation by common excitatory inputs to these motor neurons. Magnitude of synchronization is calculated from peaks in cross-correlation histograms between motor unit discharge trains. However, there are many different methods for detecting these peaks and even more indices for calculating synchronization from them. Methodology is diverse, typically laboratory-specific and requires expensive software, like Matla

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Roshchina, L. V., D. A. Gladchenko, E. A. Pivovarova та A. A. Chelnokov. "Effect of Long-Term Electrical Spinal Cord Stimulation on Expression of Non-Reciprocal Inhibition α-Motoneurons of Human Skeletal Muscles". RUDN Journal of Medicine 23, № 4 (2019): 390–96. http://dx.doi.org/10.22363/2313-0245-2019-23-4-390-396.

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It is known, transcutaneous electrical spinal cord stimulation (tESCS) in the T11-T12 level of the thoracic vertebrae increases the power capabilities of the leg agonist muscles. One of the inhibition spinal mechanisms that protects skeletal muscles from excessive force is non-reciprocal inhibition. Taking into account the biological role of non-reciprocal inhibition, the aim of the study was to research the effect of long-term tESCS on expression of non-reciprocal inhibition of soleus muscle α-motorneurons in humans at rest and when holding a weak static force. Materials and methods: the stud

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MATSUMOTO, KOJI. "Observation of motorneuron after recovery from experimental facial nerve paralysis." Nippon Jibiinkoka Gakkai Kaiho 95, no. 3 (1992): 373–80. http://dx.doi.org/10.3950/jibiinkoka.95.373.

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Brusés, Juan L., and Urs Rutishauser. "Regulation of Neural Cell Adhesion Molecule Polysialylation: Evidence for Nontranscriptional Control and Sensitivity to an Intracellular Pool of Calcium." Journal of Cell Biology 140, no. 5 (1998): 1177–86. http://dx.doi.org/10.1083/jcb.140.5.1177.

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The up- and downregulation of polysialic acid–neural cell adhesion molecule (PSA–NCAM) expression on motorneurons during development is associated respectively with target innervation and synaptogenesis, and is regulated at the level of PSA enzymatic biosynthesis involving specific polysialyltransferase activity. The purpose of this study has been to describe the cellular mechanisms by which that regulation might occur. It has been found that developmental regulation of PSA synthesis by ciliary ganglion motorneurons is not reflected in the levels of polysialyltransferase-1 (PST) or sialyltrans

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