Academic literature on the topic 'Motor neurons'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Motor neurons.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Motor neurons"

1

Tamarkin, D. A., and R. B. Levine. "Synaptic interactions between a muscle-associated proprioceptor and body wall muscle motor neurons in larval and Adult manduca sexta." Journal of Neurophysiology 76, no. 3 (September 1, 1996): 1597–610. http://dx.doi.org/10.1152/jn.1996.76.3.1597.

Full text
Abstract:
1. Synaptic remodeling of a proprioceptive circuit during metamorphosis of the insect, Manduca sexta, is described. The stretch receptor organ is a muscle-associated proprioceptor that is innervated by a single sensory neuron. It inserts dorsolaterally in the abdomen in parallel with the intersegmental muscles of each abdominal segment. The synaptic input from the stretch receptor sensory neuron to select abdominal internal (intersegmental) and external muscle motor neurons was characterized in both the larva and adult. 2. In the larva, the sensory neuron provides excitatory synaptic input to motor neurons that innervate muscles ipsilateral to the stretch receptor organ in the body wall; the strongest excitatory synaptic input is to motor neurons that innervate targets in close proximity to the stretch receptor organ. The sensory neuron also provides excitatory synaptic input to motor neurons that innervate contralateral, dorsal targets. However, it inhibits, apparently through a polysynaptic pathway, motor neurons innervating contralateral, lateral, and ventral targets. 3. The synaptic input to intersegmental muscle motor neurons from the stretch receptor sensory neuron changes during metamorphosis. In contrast to the larva, all motor neurons recorded in the adult (both ipsilateral and contralateral) were excited by the sensory neuron. As in the larva, the adult sensory neuron provides the strongest excitatory synaptic input to motor neurons innervating targets in close proximity to the stretch receptor organ. 4. The proprioceptive input to the body wall muscle motor neurons was evaluated to determine whether the pathway is monosynaptic, as has been described in other systems. Spike-triggered signal averaging and synaptic latency measurements suggested that the strongest excitatory synaptic input to motor neurons involves a monosynaptic pathway.
APA, Harvard, Vancouver, ISO, and other styles
2

Liu, Wenshu, J. Franklin Bailey, Visaka Limwongse, and Mark DeSantis. "Scanning Electron Microscopy of neuronal cell bodies isolated from the adult mammalian central nervous system." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 426–27. http://dx.doi.org/10.1017/s0424820100159679.

Full text
Abstract:
Action potentials generated in a motor neuron reflect the summation of synaptic inputs it receives from other neurons. Those synapses occur at points of contiguity between the presynaptic boutons and the surface of the motor neuron. Evidence that the density of axosomalic boutons on motor neurons varies directly with the size of the motor neuronal soma is indirect. Counts of the number of boutons per unit area at the surface of the motor neuron’s cell body using scanning electron microscopy (SEM) would allow an independent, direct assessment of that inference. We describe here procedures for consistently isolating the somas of CNS neurons, specifically those associated with the adult rat’s trigeminal nerve, so that axosomatic boutons can be seen by SEM (Figures 1 and 2).Adult male and female rats were anesthetized and then perfused with saline followed by 4% paraformaldehyde. The brain stem was removed and sectioned at 200 um thickness on a vibratome. Sections containing the trigeminal motor and mesencephalic nuclei were pinned to Sylgard-lined dishes containing phosphate buffer (0.1 M, pH 7.2).
APA, Harvard, Vancouver, ISO, and other styles
3

Church, P. J., and P. E. Lloyd. "Activity of multiple identified motor neurons recorded intracellularly during evoked feedinglike motor programs in Aplysia." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1794–809. http://dx.doi.org/10.1152/jn.1994.72.4.1794.

Full text
Abstract:
1. The firing patterns of 22 motor neurons were determined by simultaneously recording intracellularly from up to 7 neurons during evoked feedinglike buccal motor programs (BMPs). Intracellular stimulation of cerebral-buccal interneuron 2 (CBI-2) or tactile stimulation of the odontophore were used to elicit BMPs in a reduced preparation. 2. Evoked BMPs were identified as either ingestive-like (iBMP) or egestive-like (eBMP) on the basis of their similarity to those previously recorded in select neurons in freely behaving animals. Neurons were divided into the p-group, r-group, or c-group, on the basis of the phase relationships of rhythmic membrane depolarizations and hyperpolarizations during evoked BMPs. Depolarization of the p-, r-, and c-group neurons was associated with radular protraction, retraction, and closure, respectively. With one exception, the motor neurons segregated into the same groups during iBMPs and eBMPs. The exception, B7, was categorized as a c-group neuron during iBMPs, but as an r-group neuron during eBMPs. 3. Every motor neuron exhibited cyclic membrane depolarizations and hyperpolarizations, and over one-half of the neurons fired bursts of action potentials, during both iBMPs and eBMPs. The neurons fired in patterns that would be likely to release both their conventional and peptide transmitters. 4. A marked hyperpolarizing step in the p-group neurons coincident with a depolarization in the r-group neurons was observed during both iBMPs and eBMPs, suggesting a degree of shared premotor circuitry for the two BMPs. 5. A shift in the timing of activity in c-group neurons relative to that in p- and r-group neurons during iBMPs and eBMPs was observed and correlates well with the shift in phase of radular closure relative to protraction and retraction, which is useful in distinguishing ingestion from egestion in the behaving animal. 6. The firing patterns recorded in neurons that innervate overlapping populations of muscle fibers suggested that there would be complex interactions of multiple transmitters. This is particularly intriguing in the case of I3a muscle fibers, which are innervated by two excitatory and one inhibitory neuron. The firing patterns recorded in these neurons suggest that the inhibitory motor neuron may serve to not only block inappropriate contractions, but also to specifically shape evoked contractions during feeding.
APA, Harvard, Vancouver, ISO, and other styles
4

Liu, Zhiping, and Lee J. Martin. "Isolation of Mature Spinal Motor Neurons and Single-cell Analysis Using the Comet Assay of Early Low-level DNA Damage Induced In Vitro and In Vivo." Journal of Histochemistry & Cytochemistry 49, no. 8 (August 2001): 957–72. http://dx.doi.org/10.1177/002215540104900804.

Full text
Abstract:
We developed an isolation technique for motor neurons from adult rat spinal cord. Spinal cord enlargements were discretely microdissected into ventral horn tissue columns that were trypsin-digested and subjected to differential low-speed centrifugation to fractionate ventral horn cell types. A fraction enriched in α-motor neurons was isolated. Motor neuron enrichment was verified by immunofluorescence for choline acetyltransferase and prelabeling axon projections to skeletal muscle. Adult motor neurons were isolated from naïve rats and were exposed to oxidative agents or were isolated from rats with sciatic nerve lesions (avulsions). We tested the hypothesis, using single-cell gel electrophoresis (comet assay), that hydrogen peroxide, nitric oxide, and peroxynitrite exposure in vitro and axotomy in vivo induce DNA damage in adult motor neurons early during their degeneration. This study contributes three important developments in the study of motor neurons. It demonstrates that mature spinal motor neurons can be isolated and used for in vitro models of motor neuron degeneration. It shows that adult motor neurons can be isolated from in vivo models of motor neuron degeneration and evaluated on a single-cell basis. This study also demonstrates that the comet assay is a feasible method for measuring DNA damage in individual motor neurons. Using these methods, we conclude that motor neurons undergoing oxidative stress from reactive oxygen species and axotomy accumulate DNA damage early in their degeneration. (J Histochem Cytochem 49:957–972, 2001)
APA, Harvard, Vancouver, ISO, and other styles
5

Genc, Baris, Oge Gozutok, Nuran Kocak, and P. Hande Ozdinler. "The Timing and Extent of Motor Neuron Vulnerability in ALS Correlates with Accumulation of Misfolded SOD1 Protein in the Cortex and in the Spinal Cord." Cells 9, no. 2 (February 22, 2020): 502. http://dx.doi.org/10.3390/cells9020502.

Full text
Abstract:
Understanding the cellular and molecular basis of selective vulnerability has been challenging, especially for motor neuron diseases. Developing drugs that improve the health of neurons that display selective vulnerability relies on in vivo cell-based models and quantitative readout measures that translate to patient outcome. We initially developed and characterized UCHL1-eGFP mice, in which motor neurons are labeled with eGFP that is stable and long-lasting. By crossing UCHL1-eGFP to amyotrophic lateral sclerosis (ALS) disease models, we generated ALS mouse models with fluorescently labeled motor neurons. Their examination over time began to reveal the cellular basis of selective vulnerability even within the related motor neuron pools. Accumulation of misfolded SOD1 protein both in the corticospinal and spinal motor neurons over time correlated with the timing and extent of degeneration. This further proved simultaneous degeneration of both upper and lower motor neurons, and the requirement to consider both upper and lower motor neuron populations in drug discovery efforts. Demonstration of the direct correlation between misfolded SOD1 accumulation and motor neuron degeneration in both cortex and spinal cord is important for building cell-based assays in vivo. Our report sets the stage for shifting focus from mice to diseased neurons for drug discovery efforts, especially for motor neuron diseases.
APA, Harvard, Vancouver, ISO, and other styles
6

Page, Keri L., Jure Zakotnik, Volker Dürr, and Thomas Matheson. "Motor Control of Aimed Limb Movements in an Insect." Journal of Neurophysiology 99, no. 2 (February 2008): 484–99. http://dx.doi.org/10.1152/jn.00922.2007.

Full text
Abstract:
Limb movements that are aimed toward tactile stimuli of the body provide a powerful paradigm with which to study the transformation of motor activity into context-dependent action. We relate the activity of excitatory motor neurons of the locust femoro-tibial joint to the consequent kinematics of hind leg movements made during aimed scratching. There is posture-dependence of motor neuron activity, which is stronger in large amplitude (putative fast) than in small (putative slow and intermediate) motor neurons. We relate this posture dependency to biomechanical aspects of the musculo-skeletal system and explain the occurrence of passive tibial movements that occur in the absence of agonistic motor activity. There is little recorded co-activation of antagonistic tibial extensor and flexor motor neurons, and there is differential recruitment of proximal and distal flexor motor neurons. Large-amplitude motor neurons are often recruited soon after a switch in joint movement direction. Motor bursts containing large-amplitude spikes exhibit high spike rates of small-amplitude motor neurons. The fast extensor tibiae neuron, when recruited, exhibits a pattern of activity quite different to that seen during kicking, jumping, or righting: there is no co-activation of flexor motor neurons and no full tibial flexion. Changes in femoro-tibial joint angle and angular velocity are most strongly dependent on variations in the number of motor neuron spikes and the duration of motor bursts rather than on firing frequency. Our data demonstrate how aimed scratching movements result from interactions between biomechanical features of the musculo-skeletal system and patterns of motor neuron recruitment.
APA, Harvard, Vancouver, ISO, and other styles
7

Khan, Mudassar N., Pitchaiah Cherukuri, Francesco Negro, Ashish Rajput, Piotr Fabrowski, Vikas Bansal, Camille Lancelin, et al. "ERR2 and ERR3 promote the development of gamma motor neuron functional properties required for proprioceptive movement control." PLOS Biology 20, no. 12 (December 21, 2022): e3001923. http://dx.doi.org/10.1371/journal.pbio.3001923.

Full text
Abstract:
The ability of terrestrial vertebrates to effectively move on land is integrally linked to the diversification of motor neurons into types that generate muscle force (alpha motor neurons) and types that modulate muscle proprioception, a task that in mammals is chiefly mediated by gamma motor neurons. The diversification of motor neurons into alpha and gamma types and their respective contributions to movement control have been firmly established in the past 7 decades, while recent studies identified gene expression signatures linked to both motor neuron types. However, the mechanisms that promote the specification of gamma motor neurons and/or their unique properties remained unaddressed. Here, we found that upon selective loss of the orphan nuclear receptors ERR2 and ERR3 (also known as ERRβ, ERRγ or NR3B2, NR3B3, respectively) in motor neurons in mice, morphologically distinguishable gamma motor neurons are generated but do not acquire characteristic functional properties necessary for regulating muscle proprioception, thus disrupting gait and precision movements. Complementary gain-of-function experiments in chick suggest that ERR2 and ERR3 could operate via transcriptional activation of neural activity modulators to promote a gamma motor neuron biophysical signature of low firing thresholds and high firing rates. Our work identifies a mechanism specifying gamma motor neuron functional properties essential for the regulation of proprioceptive movement control.
APA, Harvard, Vancouver, ISO, and other styles
8

Quinlan, E. M., K. Gregory, and A. D. Murphy. "An identified glutamatergic interneuron patterns feeding motor activity via both excitation and inhibition." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 945–56. http://dx.doi.org/10.1152/jn.1995.73.3.945.

Full text
Abstract:
1. Previously we demonstrated that glutamate is an important neurotransmitter in the CNS of Helisoma. Exogenous glutamate applied to the buccal ganglia mimicked both the excitatory and inhibitory effects of subunit 2 (S2) of the tripartite central pattern generator (CPG) on S2 postsynaptic motor neurons. Here we identify buccal interneuron B2 as an S2 interneuron by utilizing a combination of electrophysiology, pharmacology, and intracellular staining. In addition, neurons that were electrophysiologically and morphologically characterized as neuron B2 demonstrated antiglutamate immunoreactivity, suggesting that neuron B2 is a source of endogenous glutamate in the buccal ganglia. 2. Depolarization of neuron B2 evoked excitatory postsynaptic potentials in motor neurons excited by S2. The excitatory effects of B2 depolarization and S2 activation were reversibly antagonized by the ionotropic glutamate receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione, similar to the antagonism shown previously for application of exogenous glutamate. Depolarization of neuron B2 also evoked inhibitory postsynaptic potentials in motor neurons inhibited by S2. When such motor neurons were maintained in isolated cell culture, application of exogenous glutamate produced a direct hyperpolarization of the membrane potential. 3. The activity of neuron B2 is necessary for the production of the standard pattern of buccal motor neuron activity, which underlies functional feeding movements. The subunits of the tripartite buccal CPG must be active in the temporal sequence S1-S2-S3 to produce the standard feeding pattern. Rhythmic inhibition from neuron B2 terminated activity in S1 postsynaptic motor neurons and entrained the frequency of activity in S3 postsynaptic motor neurons. Hyperpolarization of neuron B2 disrupted the production of the standard motor pattern by eliminating S2 postsynaptic potentials in identified buccal motor neurons, thereby prolonging S1 activity and disrupting S3 bursting. 4. These data support the hypothesis that S2 neuron B2 is glutamatergic and demonstrate that glutamatergic transmission, and especially inhibition, is fundamental to the production of behaviorally critical motor neuron activity patterns in Helisoma.
APA, Harvard, Vancouver, ISO, and other styles
9

Seki, Soju, Yoshihiro Kitaoka, Sou Kawata, Akira Nishiura, Toshihiro Uchihashi, Shin-ichiro Hiraoka, Yusuke Yokota, Emiko Tanaka Isomura, Mikihiko Kogo, and Susumu Tanaka. "Characteristics of Sensory Neuron Dysfunction in Amyotrophic Lateral Sclerosis (ALS): Potential for ALS Therapy." Biomedicines 11, no. 11 (November 3, 2023): 2967. http://dx.doi.org/10.3390/biomedicines11112967.

Full text
Abstract:
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder characterised by the progressive degeneration of motor neurons, resulting in muscle weakness, paralysis, and, ultimately, death. Presently, no effective treatment for ALS has been established. Although motor neuron dysfunction is a hallmark of ALS, emerging evidence suggests that sensory neurons are also involved in the disease. In clinical research, 30% of patients with ALS had sensory symptoms and abnormal sensory nerve conduction studies in the lower extremities. Peroneal nerve biopsies show histological abnormalities in 90% of the patients. Preclinical research has reported several genetic abnormalities in the sensory neurons of animal models of ALS, as well as in motor neurons. Furthermore, the aggregation of misfolded proteins like TAR DNA-binding protein 43 has been reported in sensory neurons. This review aims to provide a comprehensive description of ALS-related sensory neuron dysfunction, focusing on its clinical changes and underlying mechanisms. Sensory neuron abnormalities in ALS are not limited to somatosensory issues; proprioceptive sensory neurons, such as MesV and DRG neurons, have been reported to form networks with motor neurons and may be involved in motor control. Despite receiving limited attention, sensory neuron abnormalities in ALS hold potential for new therapies targeting proprioceptive sensory neurons.
APA, Harvard, Vancouver, ISO, and other styles
10

Bax, Monique, Jessie McKenna, Dzung Do-Ha, Claire H. Stevens, Sarah Higginbottom, Rachelle Balez, Mauricio e. Castro Cabral-da-Silva, et al. "The Ubiquitin Proteasome System Is a Key Regulator of Pluripotent Stem Cell Survival and Motor Neuron Differentiation." Cells 8, no. 6 (June 13, 2019): 581. http://dx.doi.org/10.3390/cells8060581.

Full text
Abstract:
The ubiquitin proteasome system (UPS) plays an important role in regulating numerous cellular processes, and a dysfunctional UPS is thought to contribute to motor neuron disease. Consequently, we sought to map the changing ubiquitome in human iPSCs during their pluripotent stage and following differentiation to motor neurons. Ubiquitinomics analysis identified that spliceosomal and ribosomal proteins were more ubiquitylated in pluripotent stem cells, whilst proteins involved in fatty acid metabolism and the cytoskeleton were specifically ubiquitylated in the motor neurons. The UPS regulator, ubiquitin-like modifier activating enzyme 1 (UBA1), was increased 36-fold in the ubiquitome of motor neurons compared to pluripotent stem cells. Thus, we further investigated the functional consequences of inhibiting the UPS and UBA1 on motor neurons. The proteasome inhibitor MG132, or the UBA1-specific inhibitor PYR41, significantly decreased the viability of motor neurons. Consistent with a role of the UPS in maintaining the cytoskeleton and regulating motor neuron differentiation, UBA1 inhibition also reduced neurite length. Pluripotent stem cells were extremely sensitive to MG132, showing toxicity at nanomolar concentrations. The motor neurons were more resilient to MG132 than pluripotent stem cells but demonstrated higher sensitivity than fibroblasts. Together, this data highlights the important regulatory role of the UPS in pluripotent stem cell survival and motor neuron differentiation.
APA, Harvard, Vancouver, ISO, and other styles

Dissertations / Theses on the topic "Motor neurons"

1

PLETTO, Daniela Rita. "CHARACTERIZATION OF MOLECULAR ISOFORMS AND ROLE OF THE SURVIVAL MOTOR NEURON (SMN) IN MOTOR NEURONS DISEASES." Doctoral thesis, Università degli Studi di Palermo, 2014. http://hdl.handle.net/10447/91238.

Full text
Abstract:
La sclerosi Laterale Amiotrofica (SLA) e l'Atrofia Muscolare Spinale (SMA) sono malattie neurodegenerative caratterizzate dalla perdita progressiva dei motoneuroni. La SMA è generalmente causata da delezione in omozigosi o mutazione del gene SMN, che codifica per una proteina ubiquitaria e multifunzionale, altamente espressa nel midollo spinale. La SLA è una malattia che può essere familiare o sporadica.Il 20% dei casi familiari è causato da una mutazione dominante nel gene SOD1. Inoltre ci sono altri geni coinvolti in questa malattia, tra cui FUS e TDP43. Lo scopo principale della tesi è quello di studiare il gene, le isoforme, la localizzazione subcellulare ed i partners molecolari di SMN. Inoltre, poiché sia FUS che TDP43 possiedono domini ricchi in glicina e questi sono necessari per l’interazione con SMN, sono state valutate le possibili interazioni, in modo da capire se le mutazioni dei rispettivi geni possano avere una ricaduta sulle loro interazioni e quindi sulla loro funzione. Dagli studi di RFLP-PCR, eseguiti su DNA estratto da campioni di sangue intero di pazienti SLA e di controlli neurologici, si evince che non c’è delezione a carico dell’esone 7 del gene SMN. Invece lo studio della proteina, attraverso Western blotting, ha rivelato la presenza di diverse isoforme, sia a livello nucleare che citoplasmatico di leucociti, di cellule HeLa e di cellule di neuroblastoma (SH-SY5Y). Anche le proteine TDP43 e FUS presentano diverse isoforme negli stessi campioni. Inoltre, studi di co-immunoprecipitazione SMN/FUS, fatti su cellule SH-SY5Y, hanno permesso di capire che le due proteine interagiscono a livello nucleare e nello specifico SMN interagisce con una specifica isoforma di FUS. Poi, attraverso immunofluorescenza, è stata valutata la localizzazione delle proteine studiate in cellule Hela, SH-SY5Y ed in fibroblasti umani; la distribuzione delle proteine rimane sempre la stessa nei 3 tipi cellulari : FUS in nucleoplasma, TDP43 in nucleoplasma e citoplasma, SMN in nucleoplasma, citoplasma e GEMS. Inoltre la localizzazione di FUS e di SMN e la loro interazione non cambia durante il differenziamento delle cellule di neuroblastoma in cellule neuroni-simili attraverso trattamento con acido retinoico e pretrattamento con polilisina/poliornitina. Invece la distribuzione di FUS cambia in fibroblasti umani provenienti da biopsia cutanea di un soggetto asintomatico con mutazione P525L nel gene FUS. In tali cellule la proteina FUS localizza sia nel nucleo che nel citoplasma ma anche in alcuni granuli citoplasmatici. Il fatto che FUS traslochi nel citoplasma in caso di mutazione era già stato visto in precedenza in pazienti affetti da SLA, noi qui dimostriamo per la prima volta che avviene lo stesso fenomeno in un caso pre-clinico.
The Amyotrophic Lateral Sclerosis (ALS) and the Spinal Muscular Atrophy (SMA) are neurodegenerative disorders characterized by progressive loss of motor neurons. The SMA is generally caused by homozygous deletion or mutation of the SMN gene, which encodes for a protein that is ubiquitous and multifunctional and it is highly expressed in the spinal cord. The ALS is a familial or a sporadic disease. The 20% of the cases of the familial ALS is caused by a dominant mutation in the SOD1 gene. In addition FUS and TARDBP are two other genes involved in this disease. The purpose of my thesis is to study the gene, the isoforms, the subcellular localization and the molecular partners of SMN protein. We studied the SMN gene by RFLP-PCR and we discovered that there is not deletion in exon 7 and in exon 8 of this gene. Therefore, SMN is not implicated in the pathogenesis of ALS at genetic level, for this reason we analyzed the SMN protein. We chose also two other proteins, FUS and TDP-43 because they have the prerequisites for interacting with SMN protein; in fact they have a rich in glycine domains and this is fundamental for the interaction with the SMN protein. Our studies revealed that the proteins analyzed have different isoforms. In addition we found that SMN and TDP-43 proteins are both in the nucleus and in the cytoplasm, conversely the FUS protein is only in the nucleus. We subsequently evaluated the interaction of the SMN with the FUS protein by co-immunoprecipitation. It showed that only a specific isoform of FUS interacts with the SMN protein and this interaction occurs only in the nucleus. Then we understood that the localization of the FUS and the SMN proteins and their interaction does not change during differentiation of neuroblastoma cells (SH-SY5Y) into neuronal-like adult cells by retinoic acid treatment and pretreatment with poly-lysine/poly-ornithine. Conversely, the localization of the FUS protein changes in human fibroblasts, taken from skin biopsy of an asymptomatic subject with P525L FUS mutation. In these cells the FUS protein is found both in the nucleus and in the cytoplasm. The translocation of mutated FUS from the nucleus to the cytoplasm has already been discovered by other authors in patients with amyotrophic lateral sclerosis. Here we show, for the first time, that the same phenomenon is present in a subject with FUS mutation but asymptomatic.
APA, Harvard, Vancouver, ISO, and other styles
2

Christou, Yiota Apostolou. "Generation of motor neurons from embryonic stem cells : application in studies of the motor neuron disease mechanism." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505426.

Full text
Abstract:
Embryonic stem cells are pluripotent cells with the potential to differentiate into any cell type in the presence of appropriate stimulatory factors and environmental cues. Their broad developmental potential has led to the proposal that in the future, the use of human embryonic stem cells or their differentiated progeny may be beneficial in regenerative medicine. In particular, a current goal in the field of clinical neurology is to use stem cells in cell-based therapies for motor neuron disease (MND) or amyotrophic lateral ~clerosis. MND is a progressive neurodegenerative disease that specifically affects upper and lower motor neurons and leads ultimately to death from respiratory failure. Stem cellderived motor neurons could conceivably be used to replace the degenerated cells, to provide authentic substrates for drug development and screening and for furthering our understanding of disease mechanisms. However, to reliably and accurately culture motor neurons, the complex pathways by which differentiation occurs in vivo must be understood and reiterated in vitro to direct embryonic stem cells towards motor neurons. This thesis presents the work I have performed on the directed differentiation of embryonic stem cells towards motor neuron fates. I describe the various experimental approaches I took in attempts to produce motor neurons in vitro. My studies reveal that it is possible to deploy the signals used during normal development to direct the differentiation of both human and mouse embryonic stem cells into neural and neuronal cells, including motor neurons. Two major limitations precluded my analysis of pure motor neuron cultures: first, the high concentrations of the ventralising morphogen, SHH, apparently required to direct embryonic stem cells towards motor neuron fates, and second, the difficulties encountered in culturing purified motor neurons. However, using a mixed culture, I obtained evidence that motor neurons and their progenitors fail to survive in medium conditioned by mutant SOD1-G93A astrocytes.
APA, Harvard, Vancouver, ISO, and other styles
3

Shaw, Ivan Ting-kun. "Cell death in motor neurons, two complementary models." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0028/NQ50259.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Shaw, Ivan Ting-kun 1966. "Cell death in motor neurons : two complementary models." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35486.

Full text
Abstract:
Target-dependent cell death is an important embryogenic mechanism for regulating and sculpting the developing motor system. Efficient characterization of apoptosis has been more difficult in the nervous system than in other systems due to the use of several different primary culture systems as well as with heterogeneity of neuronal cell populations. We have developed a simple in vitro model of apoptosis with the motor neuron hybrid NSC34, a cell line which expresses much of the motor neuron phenotype (Cashman et al. 1992). Serum-deprived NSC 34 cells in bulk culture undergo cell death, likely from the withdrawal of the growth factors and/or hormones present in fetal calf serum medium supplements. This cell death is accompanied by fragmentation of chromatin into nucleosome multimers, heterochromatization of the nucleus, and other ultrastructural changes reminiscent of apoptotic death. Cell death is inhibitable by addition of agents which block new gene expression ( e.g. cycloheximide) or inhibit endonuclease activity (e.g. aurintricarboxylic acid).
We report similar findings with primary embryonic rat motor neurons identified by surface immunoreactivity for p75 LA NGFR, the low-affinity neurotrophin receptor (Bloch-Gallego et al. 1991; Camu and Henderson 1992; Chao and Hempstead 1995). The p75+ motor neuron population could be maintained for more than 48 hours in mixed suspension cultures supplemented with 10% fetal calf serum. However, the p75+ cell population was rapidly depleted in serum-deprived cultures, a phenomenon accompanied by the appearance of oligonucleosomal ladders. Serum-deprived p75+ cells were supported by the motor neuron-relevant factors BDNF, CNTF, GDNF and IGF-1, but not the non-relevant factor NGF. Serum-deprived p75 + cells were also protected by cycloheximide, suggesting a role for apoptosis in the cell death.
We have investigated the role of reactive oxygen species in acquired and genetic motor neuron diseases. Interestingly, a rapid burst of reactive oxygen species is observable within one hour of serum deprivation in both NSC34 and rat motor neuron systems. This burst precedes measurable cell death by at least one day, indicating that oxygen species generation may be an initial hallmark of target-dependent death. The amplitude and temporal nature of this burst may be altered by manipulating various cellular ROS defence mechanisms. Such manipulations also alter cell death progression, suggesting that the apoptotic cascade may be dependent upon this early ROS burst. The identity, source and activity of the relevant ROS may provide insight into the etiology and treatment of human motor neuron diseases.
APA, Harvard, Vancouver, ISO, and other styles
5

Stephens, Benjamin. "Pathology of spinal interneurons in motor neuron disease." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251759.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Taylor, David M. 1977 Nov 23. "Understanding the regulation of molecular chaperones in motor neurons." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111857.

Full text
Abstract:
Cells are constantly challenged by acute and chronic stresses that must be counteracted by upregulation of protective pathways. The premise of this thesis is that motor neurons have an impaired ability to trigger these protective mechanisms, which may contribute to their preferential vulnerability in the neurodegenerative disease, amyotrophic lateral sclerosis (ALS). The first objective was to study the involvement of metallochaperones in motor neuronal stress response, including their potential for rescuing motor neurons from toxicity conferred by a mutant Cu/Zn-superoxide dismutase (SOD1G93A ) that causes a form of familial ALS. Motor neurons in dissociated spinal cord cultures failed to induce the metallochaperone, metallothionein (MT), in response to classical MT inducers, although overexpression of MT in motor neurons failed to protect them from SOD1G93A. A second response system, involving protein chaperones called heat shock proteins (Hsp), was more therapeutically promising, but was also impaired in motor neurons due to an inability to activate the regulatory protein heat shock transcription factor 1 (Hsf1). The remaining objectives were to examine if activation of Hsf1 in motor neurons would protect against SOD1G93A and to understand the mechanisms responsible for its impaired activation. A constitutively active form of Hsf1 induced multiple Hsps in motor neurons and nearly eliminated SOD1G93A toxicity and aggregation. Experiments also demonstrated that failure of stressed motor neurons to activate endogenous Hsf1 is not a result of inappropriate or insufficient activity of kinases that phosphorylate key residues of Hsf1 in nonneuronal cell lines with a competent heat shock response. Disruption of inhibitory Hsp90/multichaperone complexes is another important step in Hsf1 activation. Four different pharmacological inhibitors of Hsp90 induced multiple Hsps in motor neurons, although failure to observe the same response by targeting inhibitory complexes with activator of Hsp90 ATPase 1 (Aha1) or Daxx suggested other mechanisms were involved. A constitutively active form of calcium/calmodulin-dependent kinase N induced Hsp70 in motor neurons, but not in fibroblasts and likely through an Hsf1-independent mechanism. These results provide further evidence for disparity between the stress response of motor neurons and other cells and suggest the possibility of a unique Hsp regulatory system in neurons.
APA, Harvard, Vancouver, ISO, and other styles
7

Deinhardt, Katrin. "The endocytic pathway of tetanus neurotoxin in motor neurons." Thesis, University College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428573.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Murtha, Matthew J. III. "Transcriptional Programming of Spinal Motor Neurons from Stem Cells." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1261416295.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Wertz, Mary Helene. "Aberrant microRNA Expression in Spinal Muscular Atrophy Motor Neurons." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17464519.

Full text
Abstract:
Spinal Muscular Atrophy (SMA) is a devastating autosomal-recessive pediatric neurodegenerative disease characterized by loss of spinal motor neurons. It is caused by mutation in the survival of motor neuron 1, SMN1, gene and leads to loss of function of the full-length SMN protein. SMN has a number of functions related to RNA processing in neurons, including RNA trafficking in neurites, and RNA splicing and snRNP biogenesis in the nucleus. While previous work has focused on the alternative splicing and expression of traditional mRNAs, our lab has focused on the contribution of another RNA species, microRNAs (miRNAs), to the SMA phenotype. miRNAs are ~22 nucleotide small RNAs that are involved in post-transcriptional regulation of gene expression. They function by translational repression or mRNA decay of target RNAs. Interestingly, dysregulation of RNA processing and miRNA expression has been identified in motor neuron diseases including SMA and Amyotrophic Lateral Sclerosis. Our lab previously discovered a miRNA, miR-183, that is dysregulated in SMA and impacts its targets in cortical neurons and SMA mouse spinal cords. However, spinal motor neurons are the cell type most affected by SMN loss. We hypothesized that motor neuron specific miRNA changes are involved selective vulnerability in SMA. Therefore, we sought to determine the effect of loss of SMN on spinal motor neurons. To accomplish this, I used microarray and RNAseq to profile both miRNA and mRNA expression in primary spinal motor neurons after acute SMN knockdown. By integrating the miRNA:mRNA profiles we identified dysregulated miRNAs with enrichment in differentially expressed putative targets. miR-431 was the most substantially increased miRNA and a number of its putative targets were downregulated after SMN loss. Further, I confirm that miR-431 directly regulates its target chondrolectin and impacts neurite length. This work is critical to understanding the cell-type specific effect of aberrant miRNA expression in SMN knockdown motor neurons. It demonstrates the contribution of dysregulated RNA processing in motor neurons to neurodegeneration. Furthermore, this work highlights the impact of non-coding RNAs in human disease and points to specific miRNA whose dysregulation potentially impacts motor neuron health.
Medical Sciences
APA, Harvard, Vancouver, ISO, and other styles
10

Nakamizo, Tomoki. "Phosphodiesterase inhibitors are neuroprotective to cultured spinal motor neurons." Kyoto University, 2003. http://hdl.handle.net/2433/148692.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Motor neurons"

1

G, Stein Paul S., ed. Neurons, networks, and motor behavior. Cambridge, Mass: MIT Press, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Anthony, Taylor, Gladden M. H. 1940-, and Durbaba Rade, eds. Alpha and gamma motor systems. New York: Plenum Press, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

D, Binder Marc, and Mendell Lorne M, eds. The Segmental motor system. New York: Oxford University Press, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

M, Cochrane George, ed. The Management of motor neurone disease. Edinburgh: Churchill Livingstone, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Roger, Lemon, ed. Corticospinal function and voluntary movement. Oxford: Clarendon Press, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Roger, Lemon, ed. Corticospinal function and voluntary movement. Oxford: Oxford University Press, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Jean, Requin, Stelmach George E, North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Study Institute on Tutorials in Motor Neuroscience (1990 : Calcatoggio, France), eds. Tutorials in motor neuroscience. Dordrecht: Kluwer Academic Publishers, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Mendelsohn, Alana Irene. Specifying neurons and circuits for limb motor control. [New York, N.Y.?]: [publisher not identified], 2016.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Baek, Myungin. Development of leg motor neurons in drosophila melanogaster. [New York, N.Y.?]: [publisher not identified], 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Motor neurons"

1

Hangay, George, Susan V. Gruner, F. W. Howard, John L. Capinera, Eugene J. Gerberg, Susan E. Halbert, John B. Heppner, et al. "Motor Neurons." In Encyclopedia of Entomology, 2494. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_4707.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Guiloff, R. J. "Clinical Pharmacology of Motor Neurons." In Motor Neuron Disease, 345–73. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Roberts, P. A. "Motor Systems — Lower Motor Neurons and Pyramidal System." In Oklahoma Notes, 23–29. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2902-5_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Roberts, P. A. "Motor Systems — Lower Motor Neurons and Pyramidal System." In Oklahoma Notes, 23–29. New York, NY: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-0395-4_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Yarom, Y. "Oscillatory Behavior of Olivary Neurons." In The Olivocerebellar System in Motor Control, 209–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73920-0_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Pfaff, S. L., T. Yamada, T. Edlund, and T. M. Jessell. "Induction and Differentiation of Motor Neurons." In Neural Cell Specification, 111–24. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1929-4_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Conradi, S. "Functional Implications of Structure and Synaptology of Motor Neurons in Motor Neuron Disease." In Advances in Applied Neurological Sciences, 86–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71540-2_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Barman, S. M. "Descending Projections of Hypothalamic Sympathoexcitatory Neurons in the Cat." In Cardiorespiratory and Motor Coordination, 103–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75507-1_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Cleland, C. L., and J. A. Hoffer. "Activity of Ventral Spinocerebellar Tract Neurons Chronically Recorded in the Spinal Cord of Awake, Freely Moving Cats." In Motor Control, 155–58. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-7508-5_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Lamontagne, Angélique, and Florence Gaunet. "Social Functions of Mirror Neurons, Motor Resonance and Motor Contagion." In Revealing Behavioural Synchronization in Humans and Other Animals, 57–71. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-48449-0_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Motor neurons"

1

Ball, John M., Clarence C. Franklin, David J. Schulz, and Satish S. Nair. "Co-Regulation of Calcium and Delayed Rectifier Currents Maintains Neuronal Output in a Model of a Crustacean Cardiac Motor Neuron." In ASME 2008 Dynamic Systems and Control Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/dscc2008-2299.

Full text
Abstract:
Homeostatic processes are widespread throughout all living systems, and the nervous system is no exception. Individual neurons as well as neuronal networks must maintain levels of excitability and connectivity to ensure that consistent functional output is achieved. Possible mechanisms for maintaining functional output using co-regulation of channel conductances is studied for a motor neuron, using a computational model. The results are both consistent with and extend the biological observations.
APA, Harvard, Vancouver, ISO, and other styles
2

Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.

Full text
Abstract:
Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.
APA, Harvard, Vancouver, ISO, and other styles
3

Nicoletti, Martina, Alessandro Loppini, Letizia Chiodo, Viola Folli, Giancarlo Ruocco, and Simonetta Filippi. "Mathematical modeling of the Caenorhabditis elegans RMD motor neurons." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158182.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Vieira, Marina Duarte Gama, Anna Letícia Siqueira de Medeiros, Narayna Suellen Santos da Silva, and Edlene Lima Ribeiro. "Dysphagia in patients with amyotrophic lateral sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.398.

Full text
Abstract:
Background: Amyotrophic lateral sclerosis is a rare neurodegenerative disease that acts on the upper and lower motor neurons, causing muscle weakness.¹²³Dysphagia occurs due to malfunction of the swallowing mechanisms and generates functional problems.⁴⁵⁶ Objectives: Describe the pathophysiology of dysphagia and discuss strategies for symptom relief. Design and setting: Systematic review, Faculdade Integrada Tiradentes, Jaboatão dos Guararapes - PE. Methods: Systematic review of 10 articles from the last years. Results: Dysarthria and dysphagia are common signs of upper motor neuron involvement and 80% of ALS cases exhibit asymmetric limb weakness.⁶ Conclusions: To improve the nutrition of patients with dysphagia, is suggested the use of supplements, changes in diet and food consistency, along with education on safe swallowing modes. Also percutaneous endoscopic gastrostomy can be used as an alternative. ⁷⁸⁹¹⁰
APA, Harvard, Vancouver, ISO, and other styles
5

Elói, Daniel Vinicius, Daniel Lopes Marques de Araújo, Gabriela Fonseca Marçal, Luana Soares Vargas, Matheus Garcia Ribeiro, and Nicollas Nunes Rabelo. "Canabinoids as a therapeutic alternative in refractory epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.554.

Full text
Abstract:
Introduction: Epilepsy is characterized by abnormal electrical discharges in the brain that generate neuronal hyperexcitability and hypersynchrony. In the last years, pharmacological strategies have been efficient in the control of epileptic seizures of approximately 80% of patients, however, there are still refractory cases. Objective: To elucidate new forms of epilepsy treatment with cannabinoids. Design: Systematic Review performed at Centro Universitário Atenas – Paracatu – Minas Gerais. Methods: Literature review performed in the SciELO and PubMed databases, with the following terms: epilepsy and cannabidiol. Five papers, published from 2017 to 2020, written in English or Portuguese, were selected. Review: Epileptic seizures affect conscience, motor, sensory, and cognitive functions. The treatment with available antiepileptic drugs does not display a complete therapeutic efficiency, as it is still observed the presence of refractory patients. In this context, the cannabidiol (CBD), by interfering in the information flow between neurons, acts therapeutically preventing overload. In the central nervous system, CBD acts in the CB1 receptors, present in GABAergic inhibitory neurons and glutamatergic excitatory neurons. Evidence from an electronic research performed in 2015, with 117 parents of children with refractory epilepsy that used cannabidiol, displayed that seizures were reduced by 85%, including 14% with total suppression. Conclusion: The studies show that CBD, by acting with specific neuronal receptors, decreases cerebral hyperexcitability. Therefore, this therapeutic alternative may improve the physical and emotional well-being of refractory epileptics.
APA, Harvard, Vancouver, ISO, and other styles
6

Gonçalo, Ana Clara Mota, and Kaline dos Santos Kishishita Castro. "Treatment and main complications of Amyotrophic Lateral Sclerosis: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.520.

Full text
Abstract:
Background: Greek, the word sklerosis means hardening. In medicine, the term sclerosis refers to the stiffening of body tissues - scars. These scars (sclerosis), when located in motor neurons, are signs of Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease that affects neurons located in the primary motor cortex, brain stem, spinal cord and pyramidal tract. ALS has no cure and its treatment options are currently limited. Objectives: Review on the major complications of ALS, as well as the therapeutic methods for its treatment. Methods: Study conducted trough articles found on The New English Journal of Medicine, SpringerLink and Scholar Google and dated between 2009 and 2021. Results: ALS is known for the gradual atrophy of the muscle fibers associated with muscle loss, dysarthria and dysphagia complicated by sialorrhea, depending on the condition. All forms of the disease lead to paralysis, which causes the main consequent complication for the early mortality of patients - respiratory failure. The treatment of ALS has only one specific approved drug: riluzole, which decreases motor neuron damage, reducing disease progression and increasing patient survival. New therapeutic methods are being studied, such as treatment with stem cells and STING- induced inflammation, but they remain with limited evidence. Conclusions: ALS still has extremely restricted targeted treatment. There’s evident need for further studies aimed at a greater understanding of therapies with the potential to become effective in delaying the progression of the disease.
APA, Harvard, Vancouver, ISO, and other styles
7

Wang, Ruixue, Jiawei Han, Wang Xi, Yuhang Xu, Dingchang Zheng, Heecheon You, and Shaomin Zhang. "Calcium Activation of Parvalbumin Neurons Induced by Electrical Motor Cortex Stimulation." In 2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2022. http://dx.doi.org/10.1109/embc48229.2022.9871749.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Chae, Soyoung, Taehyung Kim, Sung-Phil Kim, Seong-Min Kim, and Jeong-Woo Sohn. "Sensory and Motor Information in Primary Motor Cortical Neurons During Arm Reaching To a Moving Target." In 2020 8th International Winter Conference on Brain-Computer Interface (BCI). IEEE, 2020. http://dx.doi.org/10.1109/bci48061.2020.9061640.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Sanggyun Kim, K. Takahashi, N. G. Hatsopoulos, and T. P. Coleman. "Information transfer between neurons in the motor cortex triggered by visual cues." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091697.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Goncharova, Polina, Natalia Shnayder, Maxim Novitsky, Regina Nasyrova, and Tatyana Davydova. "NUTRIENTS IMPACT ON MOTOR NEURONS AND THE RISK OF AMYOTROPHIC LATERAL SCLEROSIS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2088.sudak.ns2021-17/112-113.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Motor neurons"

1

Andrades, Oscar, David Ulloa, Dario Martinez, Francisco Guede, Gustava Muñoz, Luis Javier Chirosa, and Amador García. Effect of the manipulation of the variables that configure the stimulus of strength training on motor symptoms in people with Parkinson's disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0079.

Full text
Abstract:
Review question / Objective: To analyze the evidence on studies that have manipulated the variables that make up the strength training stimulus and its effects on motor symptoms in people with Parkinson's disease. Condition being studied: Parkinson's is a multisystemic neurodegenerative disease that affects the central nervous system and is caused by a loss of dopaminergic neurons in the compact part of the substantia nigra of the basal ganglia of the midbrain. People with Parkinson's disease (PEP) have non-motor and motor clinical symptoms. Classic motor symptoms are rest tremor, joint stiffness, bradykinesia, decreased balance, gait disturbances (speed, temporality, spatiality, support, and freezing) and decreased functional performance.
APA, Harvard, Vancouver, ISO, and other styles
2

Wang, Xiao, Hong Shen, Yujie Liang, Yixin Wang, Meiqi Zhang, and Hongtao Ma. Effectiveness of Tango Intervention on Motor Symptoms in Patients with Parkinson's Disease: A Protocol for Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0009.

Full text
Abstract:
Review question / Objective: Parkinson's disease (PD) is a degenerative neurological disease caused by the loss of dopaminergic neurons in the pars compacta of the substantia nigra of the brain, resulting in lesions in the basal ganglia. The main motor symptoms of PD include resting tremor, rigidity, akinesia or bradykinesia and postural instability. As an exercise intervention based on musical accompaniment, tango dance has shown positive effects on the rehabilitation of motor symptoms in PD patients in recently. In this study, we systematically reviewed the efficacy of tango intervention in alleviating the motor symptoms of patients with PD. Condition being studied: Parkinson. Information sources: The following electronic databases will be searched: PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science Core collection, and China National Knowledge Infrastructure Database (CNKI) and WanFang Database.
APA, Harvard, Vancouver, ISO, and other styles
3

Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

Full text
Abstract:
Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.
APA, Harvard, Vancouver, ISO, and other styles
4

Zhu, Qiaochu, Jin Zhou, Hai Huang, Jie Han, Biwei Cao, Dandan Xu, Yan Zhao, and Gang Chen. Risk factors associated with amyotrophic lateral sclerosis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0118.

Full text
Abstract:
Review question / Objective: To identify and list the risk factors associated with the onset and progression of ALS. Condition being studied: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting the upper and lower motor neurons in the spinal bulb, cerebral cortex, and spinal cord. The clinical processing symptoms accompany muscle atrophy, fasciculation, and fatigue of limbs, which can lead to general paralysis and death from respiratory failure within 3-5 years after the onset of this disease. Though the pathogenesis of ALS is still unclear, exploring the associations between risk factors and ALS can provide reliable evidence to find the pathogenesis in the future. This meta-analysis aims to synthesize all related risk factors on ALS, comprehensively understand this disease, and provide clues to mechanism research and clinicians.
APA, Harvard, Vancouver, ISO, and other styles
5

Zhang, Yu, Chaoliang Sun, Hengxi Xu, Weiyang Shi, Luqi Cheng, Alain Dagher, Yuanchao Zhang, and Tianzi Jiang. Connectivity-Based Subtyping of De Novo Parkinson Disease: Biomarkers, Medication Effects and Longitudinal Progression. Progress in Neurobiology, April 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.04.

Full text
Abstract:
Parkinson's disease (PD) is characterized by divergent clinical symptoms and prognosis, suggesting the presence of distinct subtypes. Identifying these subtypes is crucial for understanding the underlying pathophysiology, predicting disease progression, and developing personalized treatments. In this study, we propose a connectivity-based subtyping approach, which measures each patient's deviation from the reference structural covariance networks established in healthy controls. Using data from the Parkinson's Progression Markers Initiative, we identified two distinct subtypes of de novo PD patients: 248 patients with typical cortical-striato-thalamic dysfunctions and 41 patients showing weakened dorsal raphe nucleus (DRN)-to-cortical/striatal projections. The proposed subtyping approach demonstrated high stability in terms of random sampling of healthy or diseased population and longitudinal prediction at follow-up visits, outperforming the traditional motor phenotypes. Compared to the typical PD, patients with the DRN-predominant subtype were characterized by less server motor symptoms at baseline and distinct imaging biomarkers, including larger striatal volumes, higher concentration of cerebrospinal fluid amyloid-β and amyloid-β/t(p)-tau ratio. Subtype-specific associations and drug effects were identified that the DRN subtype exhibited more pronounced medication effects on motor symptoms, potentially regulated by DRN serotonergic modulation through striatal dopaminergic neurons. The DRN serotonergic inputs also regulated non-motor symptoms, the aggregation of CSF biomarkers and the conversion to more severe disease states. Our findings suggest that the DRN-predominant subtype represents a unique clinical and biological phenotype of PD characterized by an enhanced response to anti-parkinsonian treatment, more favorable prognosis and slower progression of dopamine depletion. This study may contribute to clinical practice of precision medicine, early invention and individualized treatments in PD and other neurodegenerative diseases.
APA, Harvard, Vancouver, ISO, and other styles
6

Santos, Ana Lúcia Yaeko da Silva, Deyse Mayara Rodrigues Caron, Livia Shirahige, and Abrahão Fontes Baptista. Alterations in Corticomotor Excitability in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0078.

Full text
Abstract:
Review question / Objective: To systematically evaluate the utility of TMS to follow up on ALS patients using neurophysiological metrics and to quantify corticomotor excitability compared to sham controls or other neuromuscular diseases. Condition being studied: Amyotrophic Lateral Sclerosis (ALS) is the third most common neurodegenerative disease (BRUNET et al., 2020). The condition is characterized by progressive muscle atrophy due to upper and lower motor neuron death (GOETZ, 2000).
APA, Harvard, Vancouver, ISO, and other styles
7

Svendsen, Clive, and Genevieve Gowing. Muscle-Derived GDNF: A Gene Therapeutic Approach for Preserving Motor Neuron Function in ALS. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada621394.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

ji, yuqin, hao tian, qiang ye, zhuoyan ye, and zeyu zheng. Effectiveness of exercise intervention on improving fundamental motor skills in children with autism spectrum disorder: A systematic review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0013.

Full text
Abstract:
Review question / Objective: This systematic review and meta-analysis aimed to synthesize available randomized controlled trial studies concerning the effects of exercise interventions on fundamental motor skills in children with autism spectrum disorder. Condition being studied: Autism Spectrum Disorder (ASD) is a complicated and highly prevalent neuro-developmental disorder characterized by deficits in social communication, restricted interests, and repetitive behaviors. The CDC reported that the prevalence of ASD was estimated to be 1 in 59 in the United States by 2020. Along with typical symptoms, a couple of studies have indicated that individuals with ASD encounter a variety of challenges, including sleep disturbance, obesity, executive function deficits, physical inactivity, and motor dysfunctions. Fundamental motor skills (FMS) are the unnaturally occurring basic motor learning model of the human body, which are the building blocks for advanced specialized motor skills and for children and adolescents to participate in sports, games, or other context-specific physical activity.FMS falls into three different categories: (a) locomotor skills (e.g., running and hopping), (b) object control skills (e.g., catching and throwing), and balance or stability skills (e.g., balancing and twisting).
APA, Harvard, Vancouver, ISO, and other styles
9

Rothstein, Jeffrey D. Anti-Excitotoxic and Antioxidant TGF-Beta Family Neurotrophic Factors: In Vitro Screening Models of Motor Neuron Degeneration. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada405360.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Performing motor and sensory neuronal conduction studies in adult humans. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, September 1990. http://dx.doi.org/10.26616/nioshpub90113.

Full text
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography