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Journal articles on the topic 'Motorneurone'

Author: Grafiati

Published: 16 November 2024

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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 (July 20, 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 sALS verlieren die Zellkerne affizierter Neurone graduell ihre Immunoreaktivität für TDP-43. Bei α-Motorneuronen entstehen unlösliche TDP-43-Einschlüsse im Zellleib, während in Betz-Zellen derartige Aggregatbildungen zunächst ausbleiben. Es erscheint daher möglich, dass in Betz-Zellen anfänglich eine im Zytoplasma noch lösliche Form des TDP-43 entsteht, die in das Axoplasma gerät, über direkte synaptische Kontakte übertragen wird und im nachfolgenden Neuron erneut die Dysregulation und Aggregation des TDP-43 auslöst. Das im Verlauf einer sALS entstehende Ausbreitungsmuster der Schädigungen ist mit der Vorstellung vereinbar, dass ein zellenschädigendes Agens über axonale Kontakte von kortikalen Projektionsneuronen auf nachfolgende Neuronen übertragen wird und dort den pathologischen Prozess erneut induziert.

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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 (March 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 (September 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 (December 1, 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 shaking-B(lethal) promoter. This construct drives reporter gene expression in the tergotrochanteral motorneuron and some other neurons. Expression of green fluorescent protein in the motorneuron allows visualization of its cell body and its subsequent intracellular staining with Lucifer Yellow. These preparations provide high-resolution data on motorneuron morphogenesis during the first half of pupal development. Dye-coupling reveals onset of gap-junction formation between the tergotrochanteral motorneuron and other neurons of the Giant-Fibre System. The medial dendrite of the tergotrochanteral motorneuron becomes dye-coupled to the peripheral synapsing interneurons between 28 and 32 hours after puparium formation. Dye-coupling between tergotrochanteral motorneuron and Giant Fibre is first seen at 42 hours after puparium formation. All dye coupling is abolished in a shaking-B(neural) mutant. To investigate any interactions between the Giant Fibre and the tergotroachanteral motorneuron, we arrested the growth of the motorneuron's medial neurite by targeted expression of a constitutively active form of Dcdc42. This results in the Giant Fibre remaining stranded at the midline, unable to make its characteristic bend. We conclude that Giant Fibre morphogenesis normally relies on fasciculation with its major motorneuronal target.

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5

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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6

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 (November 1, 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 persisted up to 18 months and is not considered to be a transient response to the trauma associated with the partial denervation. When the size of the target tissue was also reduced by extirpation of one-half of TA together with partial denervation, motorneuron size was not found to increase. It is suggested that the increase in size is a response to the metabolic demands placed upon the motorneuron by an increase in the size of the motor unit.Key words: mouse, tibialis anterior muscle, partial denervation, motorneuron size.

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8

Abbott, R. J., D. Holder, and S. Currie. "FALSE POSITIVE ANTI ACETYLCHOLINE RECEPTOR ANTIBODIES IN MOTORNEURONE DISEASE." Lancet 327, no. 8486 (April 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 (May 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 (April 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 (March 1, 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 particular lateral position, all R5 motorneuron axons must turn. In normal embryos the axons all turn rostrally to reach the nerve exit in R4. In embryos with R4 ablated, sometimes the axons turn rostrally and sometimes they turn caudally. A model combining permissive fields and chemotropic cues is presented to account for our observations.

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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 (February 1, 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 were detected on motorneuron classes DE1, DE2, DI, and VI as ACh-induced reductions in input resistance. These input resistance changes were reversed by washing in drug-free saline or by application of dTC. NMS applied alone lowered input resistance in DE1, but not in DE2, DI, or VI motorneurons. In contrast to the effect of ACh, the action of NMS in DE1 was not reversed by dTC, suggesting that NMS-sensitive sites may not respond to ACh. Excitatory synaptic responses in muscle evoked by depolarizing current injections into DE1 and DE2 motorneurons were antagonized by dTC; however, NMS antagonized the synaptic output of only the DE1 and DE3 classes of motorneurons, an effect that was more likely to have been produced by motorneuron conduction failure than by pharmacological blockade of receptor. The concentration of NMS required to produce these changes in muscle polarization and contraction, ACh antagonism, input resistance reduction, and synaptic antagonism was 100 microM, or more than five orders of magnitude higher than the binding affinity for [3H]NMS in larval Ascaris homogenates and adult Caenorhabditis elegans (Segerberg, M. A. 1989. Ph.D. thesis. University of Wisconsin-Madison, Madison, WI). These results describe a nicotinic-like pharmacology, but muscle and motorneurons also have unusual responses to muscarinic agents.

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13

SATTERLIE, RICHARD A., and ANDREW N. SPENCER. "Swimming in the Pteropod Mollusc, Clione Limacina: II. Physiology." Journal of Experimental Biology 116, no. 1 (May 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 recordings show complex subthreshold activity consisting of alternate depolarizations and hyperpolarizations. The complex activity is in antiphase in antagonistic motorneurones. Significant motor neurone-motor neurone interactions do notoccur centrally as neither electrical coupling nor chemical synaptic interactionscould be demonstrated. Injected currents do not alter the motorneurone firing rhythm or the swimming rhythm. Motor neurone cell bodies are located in the lateral region of the ipsilateralpedal ganglion, near the emergence of the wing nerve. Each motor neuroneprovides a single axon to the wing nerve which branches repeatedly in thewing. Each motor neurone has an extremely large innervation field, somecovering up to half of the wing area. The second class of pedal neurones that display firing patterns in phasewith either wing upswing or downswing are pedal-pedal inter neurones. Eachswim interneurone provides axon branches in both pedal ganglia and the axonruns in the pedal commissure. Interneurone axon branches occur in thelateral neuropile of each pedal ganglion, in the region of motor neurone branching.The swim interneurones presumably play a major role in bilateralcoordination of the wings and are involved in pattern generation since injectedcurrents were found to accelerate or slow the firing rhythms of interneuronesand motor neurones, and wing movements. Note: A significant portion of this work was conducted at Friday Harbor Laboratories, Friday Harbor, Washington, U.S.A.

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14

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 (March 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 (January 1, 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 (January 29, 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 (June 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 cords and sublateral lines. Intense staining was also present in the motorneurone commissures, indicating a potential role for NO as a neurotransmitter at the neuromuscular junction. NADPH disphorase-positive neurones were not confined to the central nervous system. Selective staining was also present in the enteric nervous system, in particular the pharynx and in the peripheral nervous system innervating the sensory organs.

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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 (March 1, 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 unusual dominant mutation, sup-41 (lb125), also co-suppresses unc-8 and deg-1, suggesting the existence of yet another common component of ion channels containing unc-8 or deg-1 subunits. Dominant, transacting, intragenic suppressor mutations have been isolated for both unc-8 and deg-1, consistent with the idea that, like their mammalian homologues, the two gene products function as multimers. The sup-40 (lb130) mutation dominantly suppresses unc-8 motorneuron swelling and produces a novel swelling phenotype in hypodermal nuclei. sup-40 may encode an ion channel component or regulator that can correct the osmotic defect caused by abnormal unc-8 channels.

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Ciriza, Jesús, Marcos García-Ojeda, Inmaculada Martín-Burriel, Cendra Agulhon, Francisco Miana-Mena, Maria Muñoz, Pilar Zaragoza, Philippe Brûlet, and Rosario Osta. "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 (June 1, 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 because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.

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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 (April 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 (PKC) and the transcription factordFoxPwere specifically involved in self-learning, but not in other forms of learning. These molecules are specifically involved in various forms of motor learning in other animals, such as compulsive biting inAplysia, song-learning in birds, procedural learning in mice or language acquisition in humans. Here we describe our efforts to decipher which PKC gene is involved in self-learning inDrosophila. We also provide evidence that motorneurons may be one part of the neuronal network modified during self-learning experiments. The collected evidence is reminiscent of one of the simplest, clinically relevant forms of motor learning in humans, operant reflex conditioning, which also relies on motorneuron plasticity.

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22

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 (May 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 conductance occurs. The hypodermal response is sodium dependent and calcium independent. Excitatory amino acid ionotropic receptor agonists (kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid and N-methyl-D-aspartate) were ineffective in eliciting hypodermal responses. The ionotropic receptor antagonist, 6,7-dinitroquinoline-2,3-dione, had no effect on hypodermal glutamate responses. The L- and D-forms of glutamate, aspartate and homocysteate produced hypodermal and DE2 depolarizations consistent with the pharmacological profile for glutamate transporters in other systems. Glutamate transport inhibitors (L-trans-pyrrolidine-2,4-dicarboxylate and beta-hydroxyaspartate) elicited electrogenic depolarizations in hypodermis and DE2. These results suggest that the hypodermal glutamate response has an electrogenic transporter component, while the DE2 response has 2 components, one conductance-mediated and the other due to an electrogenic transporter.

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23

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 (November 30, 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, antibodies against kakapo (Gregory and Brown. 1998. J. Cell Biol. 143:1271–1282) detect a specific epitope at all or most Drosophila NMJs. Within the central nervous system of kakapo mutant embryos, neuronal dendrites of the RP3 motorneuron form at correct positions, but are significantly reduced in size. At the subcellular level we demonstrate two phenotypes potentially responsible for the defects in neuronal branching: first, transmembrane proteins, which can play important roles in neuronal growth regulation, are incorrectly localized along neuronal processes. Second, microtubules play an important role in neuronal growth, and kakapo appears to be required for their organization in certain ectodermal cells: On the one hand, kakapo mutant embryos exhibit impaired microtubule organization within epidermal cells leading to detachment of muscles from the cuticle. On the other, a specific type of sensory neuron (scolopidial neurons) shows defects in microtubule organization and detaches from its support cells.

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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 (September 1988): 644–47. http://dx.doi.org/10.1016/s0140-6736(88)90467-9.

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Sabatier, Fabienne, Justine Chaigne, Maryse Martin, Rodolphe Barbeau, Luisa Houssin, Stephane Bonnin, Alastair King, and Vanessa Jahnke. "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 (March 22, 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-throughput access and a more relevant testing environment. Neuropathy is one of the most chemotherapy adverse effects. In this study we have screened 8 compounds. Bortezomib (proteasome inhibitor), gemcitabine (approved ovarian cancer treatment), ivermectin (parasitic diseases treatment), flavopiridol (approved CDKs inhibitors), SNS-032 (approved CDKs inhibitor), mefloquine (anti-malaria drug), digitonin (nonionic detergent) and tamoxifen (hormone receptor-positive breast cancer treatment). These molecule toxicities were tested on neuronal-derived iPSCs Dopaneurone, GABAneurone, Glutaneurone, Motorneurone, Microglya and Astrocytes in high throughput screening. For the project, cells were plated in 384 well/plates. DMSO tolerance was performed (up to 10%). Drugs were added, then, after 48h or 72h, total protease and protease activities were measured using CytoTox-GloTM. Compounds were tested at 7 concentrations (from 10−4 to 10−9M).In this study we have validated cell culture and the assay conditions. The signal window range was good after 48h and 72h of treatment. No toxicity was found until 10% DMSO. A specific neurotoxicity signature was measurable for each drug tested. Digitonin, our positive control, induced toxicity in all IPSCs after 48h and 72h of incubation. On the contrary, Tamoxifen, our negative control, did not induce any neurotoxicity. The other molecules generated a signature of severe to mild neurotoxicity. These results are in agreement with their known adverse side-effects. In conclusion, this panel is a good tool to anticipate possible neurotoxicity within the 3Rs respect. It can be used in early drug de-risking or neuroprotection screening, with the aim of preventing/reducing/curing neuropathy in at-risk populations. Citation Format: Fabienne Sabatier, Justine Chaigne, Maryse Martin, Rodolphe Barbeau, Luisa Houssin, Stephane Bonnin, Alastair King, Vanessa Jahnke. Neuronal cells derived from iPSCs cell to evaluate neurotoxicity after 48 or 72 hours in high-through put screening format [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7178.

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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 (June 4, 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 found that walking on a movable treadmill tape in the absence of spinal cord stimulation was accompanied by strong impulse activity of afferents I (Ia and Ib) and II groups GM, increased excitability of its motorneuron pool and weakening of afferent activity and excitability of TA. On the contrary, electrical stimulation of the spinal cord during walking caused strong impulsive activity of group II TA afferents and moderate — GM, while the activity of Ia fibers TA and GM decreased to moderate impulsivity, Ib afferents of the same muscles had the weakest activity, and the excitability of the GM motorneuron pool was greater than TA. During the postactivation period, walking was accompanied by increased impulses of afferent fibers of group Ib and II GM, weakening of afferent flows of Ib TA and Ia afferents GM, but along with this, afferent signals of group Ia and II to the motorneuron nucleus TA decreased to moderate impulses, and excitability of the motorneuron pool GM was higher than TA. The supposed reflex mechanisms of locomotion regulation are discussed on the basis of well-known phenomena associated with the interaction of various afferent inputs to the spinal cord neuronal apparatus in the system of lower leg antagonist muscles.

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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 (August 1, 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 overexpression of shh in zebrafish embryos does not induce ectopic medial floor plate cells, we conclude that shh is neither required nor sufficient to induce this cell type in the zebrafish.

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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 (September 13, 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 sequencing analysis, we identify 482 miRNAs in the regenerating central nervous system (CNS) of the mollusc Lymnaea stagnalis, 219 of which represent potentially novel miRNAs. Of the remaining conserved miRNAs, 38 show a statistically significant up- or downregulation in regenerating CNS as a result of RA treatment. We further characterized the expression of one neuronally-enriched miRNA upregulated by RA, miR-124. We demonstrate, for the first time, that miR-124 is expressed within the cell bodies and neurites of regenerating motorneurons. Moreover, we identify miR-124 expression within the growth cones of cultured ciliary motorneurons (pedal A), whereas expression in the growth cones of another class of respiratory motorneurons (right parietal A) was absent in vitro. These findings support our hypothesis that miRNAs are important regulators of retinoic acid-induced neuronal outgrowth and regeneration in regeneration-competent species.

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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 (March 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 (June 4, 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 identified heterochronic genes as major regulators of DA neuron presynaptic polarity. In many heterochronic mutants, presynapses of this cholinergic motoneuron are mislocalized to the dendrite at the ventral side: inactivation of the blmp-1 transcription factor gene, the lin-29/Zn finger transcription factor, lin-28/RNA binding protein, and the let-7miRNA gene all disrupt the presynaptic polarity of this DA cholinergic neuron. We also show that the dre-1/F box heterochronic gene functions early in development to control maintenance of polarity at later stages, and that a mutation in the let-7 heterochronic miRNA gene causes dendritic misplacement of RAB-3 presynaptic markers that colocalize with muscle postsynaptic terminals ectopically. We propose that heterochronic genes are components in the UNC-6/Netrin pathway of synaptic polarity of these neurons. These findings highlight the role of heterochronic genes in postmitotic neuronal patterning events.

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Sau, Daniela, Paola Rusmini, Valeria Crippa, Elisa Onesto, Elena Bolzoni, Antonia Ratti, and Angelo Poletti. "Dysregulation of axonal transport and motorneuron diseases." Biology of the Cell 103, no. 2 (February 2011): 87–107. http://dx.doi.org/10.1042/bc20100093.

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32

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

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33

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 (September 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 discrimination (moving and static) progressively decreased, moving down the face from the forehead to the cheek, chin, and then the lip. Sensibility thresholds are altered in patients with unilateral lower motor neuron facial nerve paresis. These findings document a relationship between sensory disturbance and lower motorneuron facial nerve paresis. The potential functional significance of this relationship has clinical significance for patients undergoing rehabilitation training. (OTOLARYNGOL HEAD NECK SURG 1993;109:506-13.)

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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 (September 1999): 531–35. http://dx.doi.org/10.1016/s0197-4580(99)00086-x.

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36

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 (May 1996): 631. http://dx.doi.org/10.1097/00005072-199605000-00115.

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37

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 (August 1989): 356–57. http://dx.doi.org/10.1016/s0140-6736(89)90538-2.

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38

Aquino-Nunez, Wendy, Zachery E. Mielko, Trae Dunn, Elise M. Santorella, Ciara Hosea, Lauren Leitner, Derrica McCalla, 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 (September 1, 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. This basic helix-loop-helix transcription factor is deeply conserved across phyla and plays a crucial role in cell fate specification in both the vertebrate nervous system and pancreas. We find that cnd-1 controls expression of ceh-5, a Vax2-like homeobox class transcription factor, in the RME head motorneurons and PVQ tail interneurons. We also show that cnd-1 functions redundantly with the Hox gene ceh-13/labial in defining the fate of DD1 and DD2 embryonic ventral nerve cord motorneurons. These data highlight the utility of comparative transcriptomes for identifying transcription factor targets and understanding gene regulatory networks.

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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 (April 1, 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 acid decarboxylase, the rate limiting enzyme of GABA synthesis in these neurons. Moreover, lim-6 gene activity and GABA signaling regulate neuroendocrine outputs of the nervous system. In the chemosensory system lim-6 regulates the asymmetric expression of a probable chemosensory receptor. lim-6 is also required in epithelial cells for uterine morphogenesis. We compare the function of lim-6 to those of other LIM homeobox genes in C. elegans and suggest that LIM homeobox genes share the common theme of controlling terminal neural differentiation steps that when disrupted lead to specific neuroanatomical and neural function defects.

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40

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 (May 1999): S136. http://dx.doi.org/10.1097/00005768-199905001-00554.

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41

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 (July 1993): 41–49. http://dx.doi.org/10.1016/0034-5687(93)90066-j.

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42

Novikov, Anton, Maria Maldova, Natalia Shandybina, Ivan Shalmiev, Elena Shoshina, Natalia Epoyan, and Tatiana Moshonkina. "First Use of Non-Invasive Spinal Cord Stimulation in Motor Rehabilitation of Children with Spinal Muscular Atrophy." Life 13, no. 2 (February 5, 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 participated in the study. They were treated with nusinersen for ~2 years. Application of tSCS was carried out during physical therapy for 30–40 min per day in the course of 10–14 days. Outcome measures were goniometry of joints with contracture, forced vital capacity (FVC), RULM and HFMSE scales. The participants tolerated the stimulation well. The reduction of the contracture was ≥5 deg. RULM and HFMSE increased by ~1–2 points. Predicted FVC increased by 1–7% in three participants. Each participant expanded their range of active movements and/or learned new motor skills. Spinal cord stimulation may be an effective rehabilitation method in patients treated with nusinersen. More research is needed.

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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 (February 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 (November 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 Matlab or LabView. This lack of standardization makes it difficult to draw definitive conclusions about motor unit synchronization. A free, open-source toolbox, “motoRneuron”, for the R programming language, has been developed which contains functions for calculating time domain synchronization using different methods found in the literature. The objective of this paper is to detail the toolbox’s functionality and present a case study showing how the same synchronization index can differ when different methods are used to compute it. A pair of motor unit action potential trains were collected from the forearm during a isometric finger flexion task using fine wire electromyography. The motoRneuron package was used to analyze the discharge time of the motor units for time-domain synchronization. The primary function “mu_synch” automatically performed the cross-correlation analysis using three different peak detection methods, the cumulative sum method, the z-score method, and a subjective visual method. As function parameters defined by the user, only first order recurrence intervals were calculated and a 1 ms bin width was used to create the cross correlation histogram. Output from the function were six common synchronization indices, the common input strength (CIS), k′, k′ − 1, E, S, and Synch Index. In general, there was a high degree of synchronization between the two motor units. However, there was a varying degree of synchronization between methods. For example, the widely used CIS index, which represents a rate of synchronized discharges, shows a 45% difference between the visual and z-score methods. This singular example demonstrates how a lack of consensus in motor unit synchronization methodologies may lead to substantially differing results between studies. The motoRneuron toolbox provides researchers with a standard interface and software to examine time-domain motor unit synchronization.

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Roshchina, L. V., D. A. Gladchenko, E. A. Pivovarova, and 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, no. 4 (December 15, 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 study involved 22 healthy male subjects aged 27 to 35 years. Non-reciprocal inhibition of α-motorneurons was recorded during the 20-minute tESCS in the T11-T12 level of the thoracic vertebrae at rest, in combination with arbitrary muscular effort (5% of MVC) and after its impact. Results: TESCS at rest resulted in the weakening of non-reciprocal inhibition within 20 minutes of exposure and 10 minutes after the end of stimulation. TESCS in combination with arbitrary muscular effort in 5% of the MVC increases the activity of non-reciprocal inhibition for 20 minutes of stimulation and 10 minutes after its end. The proposed physiological mechanisms underlying the effect of long-term tESCS on expression of non-reciprocal inhibition are discussed.

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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 (March 9, 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 sialyltransferase-X (STX) mRNA. On the other hand, PSA synthesis in both the ciliary ganglion and the developing tectum appears to be coupled to the concentration of calcium in intracellular compartments. This study documents a calcium dependence of polysialyltransferase activity in a cell-free assay over the range of 0.1–1 mM, and a rapid sensitivity of new PSA synthesis, as measured in a pulse–chase analysis of tissue explants, to calcium ionophore perturbation of intracellular calcium levels. Moreover, the relevant calcium pool appears to be within a specific intracellular compartment that is sensitive to thapsigargin and does not directly reflect the level of cytosolic calcium. Perturbation of other major second messenger systems, such as cAMP and protein kinase–dependent pathways, did not affect polysialylation in the pulse chase analysis. These results suggest that the shuttling of calcium to different pools within the cell can result in the rapid regulation of PSA synthesis in developing tissues.

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Parkes, Tony L., Andrew J. Elia, Dale Dickinson, Arthur J. Hilliker, John P. Phillips, and Gabrielle L. Boulianne. "Extension of Drosophila lifespan by overexpression of human SOD1 in motorneurons." Nature Genetics 19, no. 2 (June 1998): 171–74. http://dx.doi.org/10.1038/534.

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