Relevant bibliographies by topics / Spinal motoneuron

Academic literature on the topic 'Spinal motoneuron'

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Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Spinal motoneuron"

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Kuo, Jason J., Martijn Schonewille, Teepu Siddique, Annet N. A. Schults, Ronggen Fu, Peter R. Bär, Roberta Anelli, C. J. Heckman, and Alfons B. A. Kroese. "Hyperexcitability of Cultured Spinal Motoneurons From Presymptomatic ALS Mice." Journal of Neurophysiology 91, no. 1 (January 2004): 571–75. http://dx.doi.org/10.1152/jn.00665.2003.

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ALS (amyotrophic lateral sclerosis) is an adult-onset and deadly neurodegenerative disease characterized by a progressive and selective loss of motoneurons. Transgenic mice overexpressing a mutated human gene (G93A) coding for the enzyme SOD1 (Cu/Zn superoxide dismutase) develop a motoneuron disease resembling ALS in humans. In this generally accepted ALS model, we tested the electrophysiological properties of individual embryonic and neonatal spinal motoneurons in culture by measuring a wide range of electrical properties influencing motoneuron excitability during current clamp. There were no differences in the motoneuron resting potential, input conductance, action potential shape, or afterhyperpolarization between G93A and control motoneurons. The relationship between the motoneuron's firing frequency and injected current (f-I relation) was altered. The slope of the f-I relation and the maximal firing rate of the G93A motoneurons were much greater than in the control motoneurons. Differences in spontaneous synaptic input were excluded as a cause of increased excitability. This finding identifies a markedly elevated intrinsic electrical excitability in cultured embryonic and neonatal mutant G93A spinal motoneurons. We conclude that the observed intrinsic motoneuron hyperexcitability is induced by the SOD1 toxic gain-of-function through an aberration in the process of action potential generation. This hyperexcitability may play a crucial role in the pathogenesis of ALS as the motoneurons were cultured from presymptomatic mice.
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Quinlan, K. A., E. J. Reedich, W. D. Arnold, A. C. Puritz, C. F. Cavarsan, C. J. Heckman, and C. J. DiDonato. "Hyperexcitability precedes motoneuron loss in the Smn2B/− mouse model of spinal muscular atrophy." Journal of Neurophysiology 122, no. 4 (October 1, 2019): 1297–311. http://dx.doi.org/10.1152/jn.00652.2018.

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Spinal motoneuron dysfunction and loss are pathological hallmarks of the neuromuscular disease spinal muscular atrophy (SMA). Changes in motoneuron physiological function precede cell death, but how these alterations vary with disease severity and motoneuron maturational state is unknown. To address this question, we assessed the electrophysiology and morphology of spinal motoneurons of presymptomatic Smn2B/− mice older than 1 wk of age and tracked the timing of motor unit loss in this model using motor unit number estimation (MUNE). In contrast to other commonly used SMA mouse models, Smn2B/− mice exhibit more typical postnatal development until postnatal day (P)11 or 12 and have longer survival (~3 wk of age). We demonstrate that Smn2B/− motoneuron hyperexcitability, marked by hyperpolarization of the threshold voltage for action potential firing, was present at P9–10 and preceded the loss of motor units. Using MUNE studies, we determined that motor unit loss in this mouse model occurred 2 wk after birth. Smn2B/− motoneurons were also larger in size, which may reflect compensatory changes taking place during postnatal development. This work suggests that motoneuron hyperexcitability, marked by a reduced threshold for action potential firing, is a pathological change preceding motoneuron loss that is common to multiple models of severe SMA with different motoneuron maturational states. Our results indicate voltage-gated sodium channel activity may be altered in the disease process. NEW & NOTEWORTHY Changes in spinal motoneuron physiologic function precede cell death in spinal muscular atrophy (SMA), but how they vary with maturational state and disease severity remains unknown. This study characterized motoneuron and neuromuscular electrophysiology from the Smn2B/− model of SMA. Motoneurons were hyperexcitable at postnatal day (P)9–10, and specific electrophysiological changes in Smn2B/− motoneurons preceded functional motor unit loss at P14, as determined by motor unit number estimation studies.
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Brownstone, Robert M., and Camille Lancelin. "Escape from homeostasis: spinal microcircuits and progression of amyotrophic lateral sclerosis." Journal of Neurophysiology 119, no. 5 (May 1, 2018): 1782–94. http://dx.doi.org/10.1152/jn.00331.2017.

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In amyotrophic lateral sclerosis (ALS), loss of motoneuron function leads to weakness and, ultimately, respiratory failure and death. Regardless of the initial pathogenic factors, motoneuron loss follows a specific pattern: the largest α-motoneurons die before smaller α-motoneurons, and γ-motoneurons are spared. In this article, we examine how homeostatic responses to this orderly progression could lead to local microcircuit dysfunction that in turn propagates motoneuron dysfunction and death. We first review motoneuron diversity and the principle of α-γ coactivation and then discuss two specific spinal motoneuron microcircuits: those involving proprioceptive afferents and those involving Renshaw cells. Next, we propose that the overall homeostatic response of the nervous system is aimed at maintaining force output. Thus motoneuron degeneration would lead to an increase in inputs to motoneurons, and, because of the pattern of neuronal degeneration, would result in an imbalance in local microcircuit activity that would overwhelm initial homeostatic responses. We suggest that this activity would ultimately lead to excitotoxicity of motoneurons, which would hasten the progression of disease. Finally, we propose that should this be the case, new therapies targeted toward microcircuit dysfunction could slow the course of ALS.
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Iwagaki, Noboru, and Gareth B. Miles. "Activation of group I metabotropic glutamate receptors modulates locomotor-related motoneuron output in mice." Journal of Neurophysiology 105, no. 5 (May 2011): 2108–20. http://dx.doi.org/10.1152/jn.01037.2010.

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Fast glutamatergic transmission via ionotropic receptors is critical for the generation of locomotion by spinal motor networks. In addition, glutamate can act via metabotropic glutamate receptors (mGluRs) to modulate the timing of ongoing locomotor activity. In the present study, we investigated whether mGluRs also modulate the intensity of motor output generated by spinal motor networks. Application of the group I mGluR agonist ( S)-3,5-dihydroxyphenylglycine (DHPG) reduced the amplitude and increased the frequency of locomotor-related motoneuron output recorded from the lumbar ventral roots of isolated mouse spinal cord preparations. Whole cell patch-clamp recordings of spinal motoneurons revealed multiple mechanisms by which group I mGluRs modulate motoneuron output. Although DHPG depolarized the resting membrane potential and reduced the voltage threshold for action potential generation, the activation of group I mGluRs had a net inhibitory effect on motoneuron output that appeared to reflect the modulation of fast, inactivating Na+ currents and action potential parameters. In addition, group I mGluR activation decreased the amplitude of locomotor-related excitatory input to motoneurons. Analyses of miniature excitatory postsynaptic currents indicated that mGluRs modulate synaptic drive to motoneurons via both pre- and postsynaptic mechanisms. These data highlight group I mGluRs as a potentially important source of neuromodulation within the spinal cord that, in addition to modulating components of the central pattern generator for locomotion, can modulate the intensity of motoneuron output during motor behavior. Given that group I mGluR activation reduces motoneuron excitability, mGluRs may provide negative feedback control of motoneuron output, particularly during high levels of glutamatergic stimulation.
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Li, Y., X. Li, P. J. Harvey, and D. J. Bennett. "Effects of Baclofen on Spinal Reflexes and Persistent Inward Currents in Motoneurons of Chronic Spinal Rats With Spasticity." Journal of Neurophysiology 92, no. 5 (November 2004): 2694–703. http://dx.doi.org/10.1152/jn.00164.2004.

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In the months after spinal cord injury, motoneurons develop large voltage-dependent persistent inward currents (PICs) that cause sustained reflexes and associated muscle spasms. These muscle spasms are triggered by any excitatory postsynaptic potential (EPSP) that is long enough to activate the PICs, which take >100 ms to activate. The PICs are composed of a persistent sodium current (Na PIC) and a persistent calcium current (Ca PIC). Considering that Ca PICs have been shown in other neurons to be inhibited by baclofen, we tested whether part of the antispastic action of baclofen was to reduce the motoneuron PICs as opposed to EPSPs. The whole sacrocaudal spinal cord from acute spinal rats and spastic chronic spinal rats (with sacral spinal transection 2 mo previously) was studied in vitro. Ventral root reflexes were recorded in response to dorsal root stimulation. Intracellular recordings were made from motoneurons, and slow voltage ramps were used to measure PICs. Chronic spinal rats exhibited large monosynaptic and long-lasting polysynaptic ventral root reflexes, and motoneurons had associated large EPSPs and PICs. Baclofen inhibited these reflexes at very low doses with a 50% inhibition (EC50) of the mono- and polysynaptic reflexes at 0.26 ± 0.07and 0.25 ± 0.09 (SD) μM, respectively. Baclofen inhibited the monosynaptic reflex in acute spinal rats at even lower doses (EC50 = 0.18 ± 0.02 μM). In chronic (and acute) spinal rats, all reflexes and EPSPs were eliminated with 1 μM baclofen with little change in motoneuron properties (PICs, input resistance, etc), suggesting that baclofen's antispastic action is presynaptic to the motoneuron. Unexpectedly, in chronic spinal rats higher doses of baclofen (20–30 μM) significantly increased the total motoneuron PIC by 31.6 ± 12.4%. However, the Ca PIC component (measured in TTX to block the Na PIC) was significantly reduced by baclofen. Thus baclofen increased the Na PIC and decreased the Ca PIC with a net increase in total PIC. By contrast, when a PIC was induced by 5-HT (10–30 μM) in motoneurons of acute spinal rats, baclofen (20–30 μM) significantly decreased the PIC by 38.8 ± 25.8%, primarily due to a reduction in the Ca PIC (measured in TTX), which dominated the total PIC in these acute spinal neurons. In summary, baclofen does not exert its antispastic action postsynaptically at clinically achievable doses (<1 μM), and at higher doses (10–30 μM), baclofen unexpectedly increases motoneuron excitability (Na PIC) in chronic spinal rats.
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Daló, N. L., J. C. Hackman, K. Storey, and R. A. Davidoff. "Changes in motoneuron membrane potential and reflex activity induced by sudden cooling of isolated spinal cords: differences among cold-sensitive, cold-resistant and freeze-tolerant amphibian species." Journal of Experimental Biology 198, no. 8 (August 1, 1995): 1765–74. http://dx.doi.org/10.1242/jeb.198.8.1765.

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The effects of sudden cooling of the spinal cord were studied in three species of amphibians--a cold-sensitive tropical toad (Bufo marinus), a cold-resistant, aquatic, hibernating frog (Rana pipiens, northern leopard frog) and a freeze-tolerant frog (Rana sylvatica, wood frog). Ventral root (motoneuron) potentials were recorded from isolated, hemisected spinal cords of each species mounted in a sucrose-gap recording apparatus and superfused with HCO3(-)-buffered Ringer's solution at room temperature (21 degrees C). In the toad, sudden cooling to 6-8 degrees C produced large, sustained motoneuron depolarizations that returned slowly to baseline levels and were accompanied by extensive paroxysmal activity. Larger, but shorter-lasting, motoneuron depolarizations associated with only a limited amount of paroxysmal activity were generated by rapid cooling of the leopard frog spinal cord. Small, brief motoneuron depolarizations followed by a hyperpolarization, or hyperpolarizations not preceded by depolarizations, were seen in cooled wood frog spinal cords. The wood frog displayed a large amount of spontaneous motoneuron activity, but little paroxysmal activity in response to sudden cooling. Following prolonged cooling, rewarming the spinal cords of all three species resulted in motoneuron hyperpolarizations that slowly decayed towards the baseline value. The amplitude of the rewarming-induced response was larger and longer in toad motoneurons than in leopard frog and wood frog motoneurons. At room temperature, a single supramaximal dorsal root stimulus evoked a depolarizing ventral root potential in toad and leopard frog motoneurons that was decreased in amplitude and prolonged when the spinal cords were cooled to 8 degrees C or below. In contrast, at room temperature, the ventral root reflex in the wood frog was followed by a distinct hyperpolarization. Cooling the wood frog spinal cord only slightly reduced the amplitude of the ventral root potential. In contrast, the evoked hyperpolarization was blocked by sudden cooling and also by the addition of dihydro-ouabain to the Ringer's solution. The motoneuron hyperpolarizations induced by sudden cooling in the wood frog were converted to depolarizations when Cl- in the superfusate was replaced with isethionate. The depolarizations elicited by sudden cooling were reduced by the addition of kynurenate in all three species. A dose-response curve generated by short applications of L-glutamate demonstrated that wood frog motoneurons were less sensitive than leopard frog motoneurons to L-glutamate. In summary, three species of amphibians, differing in their adaptations to the temperature of their environments, vary in their responses to sudden reductions in temperature. The relationship of these responses to their environmental adaptations remains to be determined.
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Hochman, S., and D. A. McCrea. "Effects of chronic spinalization on ankle extensor motoneurons. I. Composite monosynaptic Ia EPSPs in four motoneuron pools." Journal of Neurophysiology 71, no. 4 (April 1, 1994): 1452–67. http://dx.doi.org/10.1152/jn.1994.71.4.1452.

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1. We examined the effects of 6-wk chronic spinalization at the L1-L2 level on composite monosynaptic Ia excitatory postsynaptic potentials (EPSPs) recorded in medial gastrocnemius (MG), lateral gastrocnemius (LG), soleus (SOL), and plantaris (PL) motoneurons. Amplitudes, rise times, and half-widths of composite monosynaptic Ia EPSPs evoked by low-strength electrical stimulation of peripheral nerves were measured in barbiturate-anesthetized cats and compared between unlesioned and chronic spinal preparations. 2. The mean amplitude of homonymous composite Ia EPSPs evoked by 1.2 times threshold (1.2T) stimulation and recorded in all four ankle extensor motoneuron pools increased 26% in chronic spinal animals compared with unlesioned controls. There was also an increased incidence of large-amplitude, short-rise time EPSPs. When the same data were separated according to individual motoneuron species, homonymous EPSP amplitudes in MG motoneurons were found to be unchanged. EPSPs recorded in LG motoneurons and evoked by stimulation of the combined LG and SOL nerve were increased by 46%. Mean EPSP amplitudes recorded in both SOL and PL motoneurons were larger after spinalization but statistical significance was only achieved when values from SOL and PL were combined to produce a larger sample size. 3. In LG motoneurons from chronic spinal animals, all EPSPs evoked by 1.2T stimulation of the LGS nerve were > or = 0.5 mV in amplitude. In unlesioned preparations, one fourth of the LG cells had EPSPs that were < or = 0.2 mV. 4. The mean amplitude of heteronymous EPSPs evoked by 2T stimulation of LGS and MG nerves and recorded in MG and LG motoneurons, respectively, doubled in size after chronic spinalization. Because homonymous EPSP amplitudes were unchanged in MG motoneurons, synaptic mechanisms and not passive membrane properties are likely responsible for increased heteronymous EPSP amplitudes in MG. 5. The mean 10-90% rise time of homonymous composite Ia EPSPs in pooled data from all motoneurons decreased 21% in 6-wk chronic spinal animals. Unlike EPSP amplitude, significant rise time decreases were found in all four motoneuron pools. Compared with the other motoneuron species, the mean homonymous rise time recorded in MG motoneurons was shortest and decreased the least in chronic spinal animals. Rise times of heteronymous Ia EPSPs in MG and LG motoneurons also decreased. The maximum rate of rise of homonymous EPSPs increased in all four motoneuron species. 6. The mean half-widths of Ia composite EPSPs decreased in 6-wk spinalized preparations in all motoneuron species.(ABSTRACT TRUNCATED AT 400 WORDS)
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Maltenfort, Mitchell G., C. J. Heckman, and W. Zev Rymer. "Decorrelating Actions of Renshaw Interneurons on the Firing of Spinal Motoneurons Within a Motor Nucleus: A Simulation Study." Journal of Neurophysiology 80, no. 1 (July 1, 1998): 309–23. http://dx.doi.org/10.1152/jn.1998.80.1.309.

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Maltenfort, Mitchell G., C. J. Heckman, and W. Zev Rymer. Decorrelating actions of Renshaw interneurons on the firing of spinal motoneurons within a motor nucleus: a simulation study. J. Neurophysiol. 80: 309–323, 1998. A simulation of spinal motoneurons and Renshaw cells was constructed to examine possible functions of recurrent inhibition. Recurrent inhibitory feedback via Renshaw cells is known to be weak. In our model, consistent with this, motoneuron firing was only reduced by a few pulses per second. Our initial hypothesis was that Renshaw cells would suppress synchronous firings of motoneurons caused by shared, dynamic inputs. Each motoneuron received an identical pattern of noise in its input. Synchrony coefficients were defined as the average motoneuron population firing relative to the activity of selected reference motoneurons; positive coefficients resulted if the motoneuron population was particularly active at the same time the reference motoneuron was active. With or without recurrent inhibition, the motoneuron pools tended to show little if any synchronization. Recurrent inhibition was expected to reduce the synchrony even further. Instead, it reduced the variance of the synchrony coefficients, without a comparable effect on the average. This suggests—surprisingly—that both positive and negative correlations between motoneurons are suppressed by recurrent inhibition. In short, recurrent inhibition may operate as a negative feedback mechanism to decorrelate motoneurons linked by common inputs. A consequence of this decorrelation is the suppression of spectral activity that apparently arises from correlated motoneuron firings due to common excitatory drive. Without recurrent inhibition, the power spectrum of the total motoneuron pool firings showed a peak at a frequency corresponding to the largest measured firing rates of motoneurons in the pool. Recurrent inhibition either reduced or abolished this peak, presumably by minimizing the likelihood of correlated firing among pool elements. Renshaw cells may act to diminish physiological tremor, by removing oscillatory components from aggregate motoneuron activity. Recurrent inhibition also improved coherence between the aggregate motoneuron output and the common drive, at frequencies above the frequency of the “synchronous” peak. Sensitivity analyses demonstrated that the spectral effect became stronger as the duration of inhibitory synaptic conductance was shortened with either the magnitude or the spatial extent of the inhibitory conductances increased to maintain constant net inhibition. Overall, Renshaw inhibition appears to be a powerful way to adjust the dynamic behavior of a neuron population with minimal impact on its static gain.
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Yamamoto, Y., J. Livet, R. A. Pollock, A. Garces, V. Arce, O. deLapeyriere, and C. E. Henderson. "Hepatocyte growth factor (HGF/SF) is a muscle-derived survival factor for a subpopulation of embryonic motoneurons." Development 124, no. 15 (August 1, 1997): 2903–13. http://dx.doi.org/10.1242/dev.124.15.2903.

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Muscle-derived factors are known to be important for the survival of developing spinal motoneurons, but the molecules involved have not been characterized. Hepatocyte growth factor/scatter factor (HGF/SF) plays an important role in muscle development and motoneuron axon outgrowth. We show that HGF/SF has potent neurotrophic activity (EC50=2 pM) for a subpopulation (40%) of purified embryonic rat motoneurons. Moreover, HGF/SF is an essential component of muscle-derived support for motoneurons, since blocking antibodies to HGF/SF specifically inhibited 65% of the trophic activity of media conditioned by C2/C7 skeletal myotubes, but did not inhibit the trophic activity secreted by Schwann cell lines. High levels of expression of the HGF/SF receptor c-Met in the spinal cord are restricted to subsets of motoneurons, mainly in limb-innervating segments. Consistent with this distribution, cultured motoneurons from limb-innervating brachial and lumbar segments showed a more potent response to HGF/SF than did thoracic motoneurons. By the end of the period of motoneuron cell death, levels of c-Met mRNA in motoneurons were markedly reduced, suggesting that the effects of HGF/SF may be limited to the period of motoneuron cell death. HGF/SF may play an important role during motoneuron development as a muscle-derived survival factor for a subpopulation of limb-innervating motoneurons.
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Smith, J. C., J. J. Greer, G. S. Liu, and J. L. Feldman. "Neural mechanisms generating respiratory pattern in mammalian brain stem-spinal cord in vitro. I. Spatiotemporal patterns of motor and medullary neuron activity." Journal of Neurophysiology 64, no. 4 (October 1, 1990): 1149–69. http://dx.doi.org/10.1152/jn.1990.64.4.1149.

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1. An analysis of the spatial and temporal patterns of activity of neurons of the respiratory motor-pattern generation system in an in vitro neonatal rat brain stem-spinal cord preparation is presented. Impulse discharge patterns of spinal and cranial moto-neurons as well as respiratory neurons in the medulla were analyzed. Patterns of motoneuronal discharge were characterized at the population level from recordings of motor-nerve discharge and at the single-cell level from intracellular recordings. These patterns were compared to patterns generated in the neonatal rat and adult mammal in vivo to establish the correspondence between in vitro and in vivo states. 2. The in vitro system generated a complex spatiotemporal pattern of spinal and cranial motoneuron activity during inspiratory (I) and expiratory (E) phases of the respiratory cycle. The respiratory cycle consisted of three distinct phases of neuronal activity (I, early E, and late E phase) similar to the temporal organization of the cycle in the intact mammal. The spike discharge pattern of motoneurons during the I phase consisted of a rapidly peaking-slowly decrementing discharge envelope with a high degree of synchronization on a time scale of 25-50 ms (approximately 20-40 Hz). A similar pattern was generated in the neonate in vivo under conditions comparable with the in vitro state (i.e., nervous system isolated from mechanosensory afferent inputs). However, the I-phase-motoneuron discharge pattern and cycle-phase durations differed from those characteristic of the intact neonatal or adult systems in vivo. This difference could be accounted for primarily by removal of vagal mechanosensory afferent inputs. 3. The synaptic drive potentials of spinal motoneurons during the I phase in vitro consisted of a rapidly peaking-slowly decrementing potential envelope similar in shape to the spike-frequency histogram of single motoneurons and the envelope of the motoneuron-population discharge. The drive potentials had prominent high-frequency amplitude fluctuations superimposed on the slower drive-potential envelope that were temporally correlated with the generation of motoneuron action potentials. The dominant frequency components of these fast-membrane-potential oscillations (20-35 Hz) were similar to the frequency components of the amplitude fluctuations in the motoneuron-population discharge. One class of medullary neurons with I-phase discharge also exhibited a rapidly peaking-slowly decrementing pattern of impulse discharge and synaptic drive potential with similar high-frequency components.(ABSTRACT TRUNCATED AT 400 WORDS)
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Dissertations / Theses on the topic "Spinal motoneuron"

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Narayan, Sreenath. "REANIMATION OF A DENERVATED MUSCLE USING UPPER MOTONEURON INJURED LOWER MOTONEURONS IN SPINAL CORD INJURY PATIENTS: A RAT MODEL." online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1133754830.

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Chopek, Jeremy W. "Lumbar spinal cord excitability: flexors vs. extensors, sensitivity to quipazine; effects of activity following spinal transection; and expression of post-synaptic serotonin receptors." American Physiological Society, 2013. http://hdl.handle.net/1993/24099.

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Serotonin (5-HT) is a well-known modulator of spinal cord excitability and motor output. In the spinal cord, the actions of 5-HT are primarily mediated by the 5-HT1AR, 5-HT2Rs and the 5-HT7R. Following a spinal cord transection, which results in a loss of supraspinal input, 5-HT agonists such as quipazine are used to provide excitation to the spinal cord to facilitate locomotor recovery. This is characterized by rhythmic alteration of left and right hindlimbs and ipsilateral flexor and extensor muscles. However, whether 5-HT has a global effect on spinal cord excitability or is confined to a specific motor group (i.e. flexors or extensors) is currently unknown. Furthermore, quipazine is used in conjunction with activity based interventions to enhance recovery following a spinal cord injury. However, the influence of limb activity on the responsiveness of the injured spinal cord to quipazine has not been examined. Lastly, the recovery of locomotion is at least in part thought to occur through an up-regulation of 5-HT receptors, although this has not been investigated in lumbar spinal cord. Chapter 2 examines whether quipazine had a differential effect on flexor and extensor motor output assessed by recording flexor and extensor reflexes, motoneurons and Ia extracellular field potentials pre- and post-quipazine. It was determined that following an acute spinal transection, quipazine induced a larger flexor monosynaptic reflex (MSR) compared to the extensor MSR due to pre-synaptic but not motoneuron modulation. Chapter 3 examines the influence of a chronic spinal transection with and without passive cycling on the hindlimb flexor and extensor MSR, both pre- and post-quipazine. It was found that three months post STx, the extensor but not flexor MSR demonstrated a hyperexcitable response, which was attenuated with passive cycling. Further, three months of passive cycling extensor MSR response to quipazine was similar to that seen in the control intact group. Chapter 4 examined 5-HT receptor expression in flexor and extensor motoneurons three months post spinalization with or without passive cycling. Following a chronic STx, the 5-HT1AR and 5-HT2CR are down regulated, whereas the 5-HT2AR is up-regulated. Passive cycling further enhanced the 5-HT2AR expression as well as up-regulated the 5-HT7R in extensor but not flexor motoneurons. Chapter 5 discusses the results and significance of these findings in detail.
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Arumugam, Saravanan. "A Study on the Role of NF-kB Signaling Pathway Members in Regulating Survival Motor Neuron Protein level and in the Pathogenesis of Spinal Muscular Atrophy." Doctoral thesis, Universitat de Lleida, 2017. http://hdl.handle.net/10803/400607.

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L’atròfia muscular espinal (AME) és una malaltia neuromuscular causada per mutació o deleció en el gen SMN1, que codifica per la proteïna ubiqua SMN (de l’anglès survival motor neuron). L’AME es caracteritza per atròfia muscular i degeneració de les motoneurones (MN) de la medul·la espinal. Els esdeveniments moleculars que causen la vulnerabilitat específica de les MN amb nivells baixos de proteïna SMN encara no es coneixen. La via de l’NF-κB (nuclear factor-κB) ha destacat recentment ja que sembla jugar un paper cabdal en la supervivència de les MN i en les malalties neurodegeneratives. Els factors de transcripció NF-κB regulen gens relacionats amb molts processos cel·lulars. En aquest treball hem analitzat la capacitat dels membres de la via de l’NF-κB de regular la proteïna Smn i el seu possible rol en la patogènesi de l’AME. L’activació de la via de l’NF-κB està associada a la fosforilació de l’IKKα/IKKβ i la translocació nuclear del factor RelA/p50 (via canònica) o la fosforilació de l’homodímer d’IKKα i la translocació nuclear del factor RelB/p52 (via no canònica). La inhibició de diferents membres d’aquestes vies (tant la canònica com la no canònica) usant la metodologia de transducció amb lentivirus amb shRNA en cultius primaris de MN embrionàries aïllades de ratolí hem demostrat que una reducció selectiva del factor RelA provoca una reducció de la proteïna Smn, mentre que una reducció del factor RelB no té cap efecte en els nivells de l’Smn. En el nostre model cel·lular, la reducció dels nivells de l’IKKα o l’IKKβ provoca un efecte oposat en l’Smn. Mitjançant la tècnica de la RT-PCR hem observat que la transducció de les MN amb l’shIKKβ provoca un augment dels nivells de l’mRNA de Smn, mentre que la transducció amb l’shIKKα o l’shRelA no modifica l’expressió de Smn. El doble knockdown de l’IKKα i l’IKKβ a les MN mostra una reducció de l’Smn. El knockdown selectiu de l’IKKα o l’IKKβ presenta una reducció de la fosforilació del RelA, es coneix que aquesta fosforilació en permet l’alliberament del seu inhibidor al citosol i en facilita la translocació nuclear. També la proteïna CREB, un dels factors de transcripció coneguts de l’Smn, disminueix amb la transducció de les MN amb els shIKKα o amb l’IKKα i l’IKKβ alhora, així com amb l’shRelA. Ara bé, les motoneurones amb l’shIKKβ mostren una reducció de la fosforilació de RelA però un augment dels nivells de CREB. La transducció de les MN amb l’shCREB disminueix els nivells de l’Smn recolzant el paper regulador de CREB en l’Smn. Hem observat una reducció de l’IKKα, l’IKKβ i de la fosforilació de RelA amb la transducció de les MN amb l’shSmn i en les MN del model murí sever de l’AME. Els nostres resultats mostren l’habilitat de la via canònica de l’NF-κB de regular els nivells de l’Smn i que aquesta via també es troba alterada en les MN deficients en la proteïna Smn. En conjunt, aquestes observacions suggereixen que la via de l’NF-κB pot tenir un rol en la patogènesi i ser, a la vegada, una possible diana terapèutica per l’AME.
La Atrofia Muscular Espinal (SMA) es un trastorno neuromuscular causado por la mutación o deleción del gen SMN1, el cual codifica para la proteína que se expresa ubicuamente SMN (del inglés Survival Motor Neuron). La AME se caracteriza por atrofia muscular y degeneración de las motoneuronas de la médula espinal (MN). Los eventos moleculares detrás de la vulnerabilidad selectiva de las MN con niveles bajos de la proteína SMN se desconocen. La vía del factor nuclear-kB (NF-kB) ha sido implicada recientemente en la supervivencia de las MNs, así como en trastornos neurodegenerativos. Los factores de transcripción NF-kB regulan genes relacionados con varios procesos celulares. En este trabajo hemos analizado la capacidad de los miembros de la vía del NF-κB de regular la proteína SMN y su posible rol en la patogénesis del AME. La activación de la vía del NF-κB está asociada a la fosforilación de IKKα / IKKβ y la translocación nuclear del factor RelA/ p50 (vía canónica) o la fosforilación del homodímero de IKKα y la translocación nuclear del factor RelB / p52 (vía no canónica). Hemos realizado la inhibición de diferentes miembros de estas vías (tanto la canónica como la no canónica) usando la metodología de shRNA, y la transducción mediante el uso de lentivirus, en cultivos primarios de MN embrionarias aisladas de ratón. Hemos demostrado que una reducción selectiva del factor RelA provoca una reducción de la proteína SMN, mientras que una reducción del factor RelB no tiene ningún efecto en los niveles de la SMN. En nuestro modelo celular, la reducción de las proteínas IKKα o IKKβ mostró efectos opuestos sobre la proteína Smn. Mediante la técnica de PCR, hemos observado que la transducción de las MN con el shIKKβ provoca un aumento de los niveles de mRNA de SMN, mientras que la transducción con el shIKKα o el shRelA no cambian los niveles de RNA de SMN. El doble knockdown de IKKα e IKKβ en las MN muestra una reducción de SMN. El knockdown selectivo de IKKα o IKKβ presenta una reducción de la fosforilación del RelA, esta fosforilación permite la liberación de su inhibidor en el citosol y facilita la translocación nuclear. La proteína CREB, uno de los factores de transcripción conocidos para SMN, disminuye con la transducción de las MN con shIKKα o con IKKα e IKKβ a la vez, así como con shRelA. Ahora bien, las motoneuronas transducidas con shIKKβ muestran una reducción de la fosforilación de RelA pero un aumento de los niveles de la proteína CREB. La transducción de las MN con el shCREB disminuyó los niveles de la proteína SMN apoyando el papel regulador de CREB sobre SMN.
Spinal Muscular Atrophy (SMA) is a neuromuscular disorder caused by mutation or loss in SMN1 gene, encoding the ubiquitously expressed Survival Motor Neuron (SMN) protein. SMA is characterized by muscle atrophy, and spinal cord motoneurons (MNs) degeneration. The molecular events behind the selective vulnerability of these MNs to low level of SMN protein are still unknown. The nuclear factor-κB (NF-κB) pathway has recently been emerged having a vital role related to MN survival, and in neurodegenerative disorders. The NF-κB transcription factors regulate genes related to several cellular processes. In the present work, we have analyzed the ability of NF-κB pathway members to regulate Smn and their possible role in SMA pathogenesis. The NF-κB pathway activation is associated with IKKα/IKKβ phosphorylation, and RelA/p50 nuclear translocation (canonical) or IKKα homodimer phosphorylation, and RelB/p52 nuclear translocation (non-canonical). The inhibition of different protein members of both canonical, and non-canonical pathways using shRNA lentiviral transduction methodology in a primary culture of isolated embryonic spinal cord MNs reveals that the selective reduction of RelA induced the reduction of Smn whereas RelB protein reduction had no effect on Smn. In our culture system, reduction of IKKα or IKKβ proteins showed opposite effects on Smn. RT-PCR studies indicate that the shIKKβ-transduced MNs showed increased Smn mRNA levels, whereas it was not observed changes in Smn mRNA in the case of shIKKα- or shRelA-transduced MNs. The double knock-down of IKKα and IKKβ in MNs showed Smn reduction. The knockdown of IKKα and/or IKKβ showed a decrease in RelA phosphorylation, where the phosphorylation of RelA enable RelA/p50 release from its inhibitor in the cytoplasm and facilitates their nuclear translocation. Also, the CREB, one of the transcription factors for Smn was decreased in shIKKα, or in shIKKα- plus IKKβ-transduced MNs, and as well as in shRelA-transduced MNs. But, the shIKKβ MNs exhibited reduced p-RelA but increased CREB level. The shCREB-transduced MNs decreased Smn level, authenticating the regulatory role of CREB on Smn. We observed a reduction in IKKα, IKKβ and p-RelA levels in shSmn-tranduced MNs, and in MNs from a severe type SMA mouse model. Our results show the ability of NF-κB canonical pathway to regulate Smn level and, conversely, this pathway is also altered in Smn-deficient MNs. Together, these observations suggest that the NF-κB pathway has a role in SMA pathogenesis, and could be a therapeutic target for SMA.
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Sowd, Matthew Michael. "Analyzing Non-Unique Parameters in a Cat Spinal Cord Motoneuron Model." Thesis, Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/11545.

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When modeling a neuron, modelers often focus on the values of parameters that produce a desired output. However, if these parameters are not unique, there could be a number of parameter sets that produce the same output. Thus, even though the values of the various maximum conductances, half activation voltages and so on differ, as a set they can produce the same spike height, firing rates, and so forth. To examine whether or not parameter sets are unique, a 3-compartment motoneuron model was created that has 15 target outputs and 59 parameters. Using parameter searches, over one hundred parameter sets were created for this model that produced the same output (within tolerances). Parameter values vary between parameter sets and indicate that the parameter values are not unique. In addition, some parameters are more tightly constrained than others. Principal component analysis is used to examine the dimensionality of the input and output spaces. However, neurons are more than static output generators. For example, a variety of neuromodulatory influences are known to shift parameter values to alter neuronal output. Thus the question arises as to whether this non-uniqueness extends from model outputs to the models sensitivities to its parameters. In this work, the non-unique parameter sets are further analyzed using sensitivity analyses and output correlations to show that these values vary significantly between these parameter sets. Therefore, each of these models will react to parameter variation differently. This work concludes that parameter sets are non-unique but have varying sensitivity analyses and output correlations. The ramifications of this are discussed for both modelers and neuroscientists.
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Rademacher, Sebastian [Verfasser]. "Cytoskeletal dysregulation in the motoneuron disease Spinal Muscular Atrophy (SMA) / Sebastian Rademacher." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2017. http://d-nb.info/1136298002/34.

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Zelano, Johan. "Adhesion molecules and synapse remodeling during motoneuron regeneration." Stockholm : Department of Neuroscience, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-623-1/.

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Van, Ryswyk Liesl, and Ryswyk Liesl Van. "A Question of Identity: Genes that Distinguish Motoneurons from Interneurons." Thesis, University of Oregon, 2012. http://hdl.handle.net/1794/12539.

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The question of how a single cell can grow, divide, and ultimately acquire a distinct function within an adult animal is central to the field of developmental biology. An elegant way to address this question is by studying the specification of a specific cell type, for example, vertebrate motoneurons. For an animal to be able to move and behave appropriately, individual motoneurons (MNs) must correctly innervate specific muscles. For this to happen, MNs must first be specified and then must differentiate into distinct subtypes, each of which is classified in part by the muscle it innervates. MN subtype specification is dependent on both the acquisition of MN-specific characteristics as well as the failure to acquire characteristics specific to interneurons, cells that only innervate other neurons. The entire process of specification is initiated in progenitor cells and relies on the correct spatial and temporal expression of specific genes. Previous work in various vertebrate models has identified some of the key genes involved in MN specification, most notably transcription factors such as olig2, nkx6s, lhxs, mnxs, and islet1. In this dissertation, I use the zebrafish model to demonstrate novel roles in MN specification for two of these families of transcription factors - the lhxs and the mnxs. I provide evidence that both lhx3 and lhx4 are necessary for normal MN and ventral interneuron (IN) development and work by preventing MNs from expressing IN-specific characteristics. I also show that mnx1, mnx2a, and mnx2b are necessary in MNs both to promote the acquisition of some MN subtype-specific characteristics and to prevent the acquisition of some IN-specific characteristics and appear to be working in part through interactions with islet1. Finally, I identify an intermediate filament gene, inab, as being expressed in a subset of zebrafish MNs and a ventral IN and as having a potential role in the axon outgrowth of a specific MN subtype. Together, this work provides evidence for a mechanism of MN specification dependent on the expression of genes that both promote aspects of MN fate and inhibit aspects of IN fate. This dissertation includes previously unpublished co-authored material.
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柴宏 and Hong Chai. "Survival and regeneration of spinal motoneuron after ventral root avulsion in adult rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B3124158X.

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Chai, Hong. "Survival and regeneration of spinal motoneuron after ventral root avulsion in adult rat /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?

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Obeidat, Ahmed Zayed. "New Insights into the Spinal Recurrent Inhibitory Pathway Normally and After Motoneuron Regeneration." Wright State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=wright1369702090.

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Books on the topic "Spinal motoneuron"

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Krammer, Eva B., Martin F. Lischka, Thomas P. Egger, Maria Riedl, and Helmut Gruber. The Motoneuronal Organization of the Spinal Accessory Nuclear Complex. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-662-10362-3.

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Mason, Peggy. Spinal Cord. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0004.

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The spinothalamic and lemniscal pathways carry somatosensory information from the periphery into the brain while the corticospinal pathway carries motor commands from the brain to motoneurons of the spinal cord. Following these pathways through the spinal cord allows the student to infer lesion location from symptoms. To exemplify the clinical importance of sympathetic outputs from thoracic segments, Horner syndrome is described. Similarly, the common problems caused by spinal cord injury on sacral parasympathetic functions are stressed. The contributions of specific spinal segments to breathing, hand and foot dexterity, and micturition are emphasized. Working through the logic of the symptoms caused by spinal hemisection (Brown-Séquard syndrome), pyramidal stroke, and syringomyelia provides the student with a clear framework for understanding spinal function in the clinical context.
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Gruber, Helmut, Eva B. Krammer, Martin F. Bach, Thomas P. Egger, and Maria Riedl. The Motoneuronal Organization of the Spinal Accessory Nuclear Complex. Springer, 1987.

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1944-, Krammer E. B., ed. The Motoneuronal organization of the spinal accessory nuclear complex. Berlin: Springer-Verlag, 1987.

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Mason, Peggy. Introduction to the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0001.

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The primary regions and principal functions of the central nervous system are introduced through the story of Jean-Dominique Bauby who became locked in after suffering a brainstem stroke. Bauby blinked out his story of locked-in syndrome one letter at a time. The primary deficit of locked-in syndrome is in voluntary movement because pathways from the brain to motoneurons in the brainstem and spinal cord are interrupted. Perception is also disturbed as pathways responsible for transforming sensory stimuli into conscious awareness are interrupted as they ascend through the brainstem into the forebrain. Homeostasis, through which the brain keeps the body alive, is also adversely affected in locked-in syndrome because it depends on the brain, spinal cord and autonomic nervous system. Abstract functions such as memory, language, and emotion depend fully on the forebrain and are intact in locked-in syndrome, as clearly evidenced by Bauby’s eloquent words.
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Mason, Peggy. Reflexes and Gait. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0022.

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The importance of proprioception to motor function is revealed by the dramatic story of Ian Waterman, a man who lost function in all proprioceptive and tactile spinal afferents. The circuitry of the stretch reflex, termed the deep tendon reflex in clinical circles, is described in detail. In this context, the student is introduced to load, muscle spindles, Ia afferents, α‎- and γ‎- motoneurons, and α‎- γ‎ coactivation. The concept of physiological extensors and flexors is useful for understanding the role of reflexes in normal and abnormal postures. The logic and utility of reflex testing is fully explained and the Ib and nociceptive withdrawal reflexes briefly introduced. Primitive reflexes and their modulation across development and in response to stroke or disease are presented. In a final segment, movements produced by central pattern generators and refined by reflexes are illustrated by a close examination of human gait across the life cycle.
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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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Book chapters on the topic "Spinal motoneuron"

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Burke, Robert. "Spinal Motoneurons." In Neuroscience in the 21st Century, 1027–62. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1997-6_33.

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Burke, Robert. "Spinal Motoneurons." In Neuroscience in the 21st Century, 1153–88. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3474-4_33.

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Adeeb, Nimer, R. Shan Tubbs, Aman Deep, and Martin M. Mortazavi. "Locomotor Recovery After Spinal Cord Transection: Transplantation of Oligodendrocytes and Motoneuron Progenitors from Human Embryonic Stem Cells." In Stem Cells and Cancer Stem Cells, Volume 13, 55–71. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7233-4_5.

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Erceg, Slaven, and Miodrag Stojkovic. "Locomotor Recovery After Spinal Cord Transection: Transplantation of Oligodendrocytes and Motoneuron Progenitors Generated from Human Embryonic Stem Cells." In Tumors of the Central Nervous System, Volume 6, 211–19. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2866-0_24.

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Powers, Randy. "Compartmental Models of Spinal Motoneurons." In Encyclopedia of Computational Neuroscience, 1–9. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-7320-6_741-1.

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Powers, Randy. "Compartmental Models of Spinal Motoneurons." In Encyclopedia of Computational Neuroscience, 660–67. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_741.

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Jiang, Z. G., and N. J. Dun. "Actions of Acetylcholine on Spinal Motoneurons." In Neurobiology of Acetylcholine, 283–93. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5266-2_23.

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Juurlink, Bernhard H. J. "Chick Spinal Somatic Motoneurons in Culture." In Protocols for Neural Cell Culture, 77–89. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2586-5_5.

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Milligan, Carol, and David Gifondorwa. "Isolation and Culture of Postnatal Spinal Motoneurons." In Methods in Molecular Biology, 77–85. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-328-8_5.

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Brock, L. G., J. S. Coombs, and J. C. Eccles. "Antidromic Propagation of Impulses into Motoneurones." In Ciba Foundation Symposium - The Spinal Cord, 120–31. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718827.ch11.

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Conference papers on the topic "Spinal motoneuron"

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Gamal, Mai, Mohamed H. Mousa, Seif Eldawlatly, and Sherif M. Elbasiouny. "Automated Cell-Type Classification and Death-Detection of Spinal Motoneurons." In 2018 9th Cairo International Biomedical Engineering Conference (CIBEC). IEEE, 2018. http://dx.doi.org/10.1109/cibec.2018.8641824.

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Mousa, Mohamed H., Ahmed H. Kandil, and Sherif M. Elbasiouny. "Simulation of dendritic L-type ca channels' warm-up phenomenon in spinal motoneurons." In 2016 8th Cairo International Biomedical Engineering Conference (CIBEC). IEEE, 2016. http://dx.doi.org/10.1109/cibec.2016.7836113.

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Abdelaal, Amr Y., Mohamed H. Mousa, Mai Gamal, Mahmoud I. Khalil, Sherif M. Elbasiouny, and Seif Eldawlatly. "A Classification Approach to Recognize the Firing of Spinal Motoneurons in Amyotrophic Lateral Sclerosis." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176551.

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Kalinina, Natalia, Aleksey Zaitsev, and Nikolai Vesselkin. "CHANGE OF THE MODULATING INFLUENCE OF SEROTONIN ON THE FUNCTIONAL PROPERTIES OF SPINAL MOTONEURONS AFTER THEIR DAMAGE." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1074.sudak.ns2020-16/238-239.

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Barra, Beatrice, Camille Roux, Melanie Kaeser, Giuseppe Schiavone, Stephanie P. Lacour, Jocelyne Bloch, Gregoire Courtine, Eric M. Rouiller, Eric Schmidlin, and Marco Capogrosso. "Selective Recruitment of Arm Motoneurons in Nonhuman Primates Using Epidural Electrical Stimulation of the Cervical Spinal Cord." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8512554.

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Kalinina, Natalia, Aleksey Zaitsev, and Nikolai Veselkin. "ROLE OF 5-HT 1B/D AND 5-HT 5A RECEPTORS IN MODULATION OF SYNAPTIC TRANSMISSION IN SPINAL MOTONEURONS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2148.sudak.ns2021-17/175-176.

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