Neural Mechanism by Which Controlling Inputs Influence Motor Output in the Flying Locust

1967 ◽  
Vol 47 (2) ◽  
pp. 213-228
Author(s):  
INGRID WALDRON
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Neural Mechanism ◽  
Sensory Nerves ◽  
Rapid Variation ◽  
Flight Pattern ◽  
Burst Length ◽  
Rapid Changes ◽  
Length Changes ◽  
Individual Motor

1. The central nervous system of the flying locust generates a pattern of alternating bursts of impulses in the elevator and depressor motor neurons (Wilson, 1961). The mechanism by which controlling inputs modify this output pattern is analysed in this paper. 2. During roll turns and other flight manoeuvres the average number of impulses per burst (average burst length) changes in certain motor neurons. Changes in average burst length develop slowly, over tens of wingbeat cycles, even in response to the abrupt changes in input which result from electrical stimulation of sensory nerves. 3. In addition to the slow changes in average burst length which are elicited by controlling inputs, more rapid changes in burst length sometimes occur. During this rapid variation a longer burst is usually followed by a shorter burst, probably because the motor neuron is less excitable after a longer burst of activity. Burst length varies independently in different motor neurons. Both findings suggest that much of the rapid variation in burst length is due to changes occurring within the individual motor neurons, and is not a response to rapid changes in controlling inputs. 4. Under all conditions, changes in the number of impulses per burst are correlated with small changes in the relative timing of the burst; the longer bursts produced by a motor neuron begin slightly earlier in the wingbeat cycle. This implies that the factors which cause variation in the length of the bursts are also responsible for producing the variation in the timing of the bursts. 5. All of the observations can be explained on one assumption: that the only effect of controlling inputs is to cause slow changes in the ‘average excitation’ of individual motor neurons. Thus sensory and central control of the flight pattern generating system appears to be slow control over the average performance, rather than fast control over performance in a particular cycle.

Motor Patterns During Flight and Warm-up in Lepidoptera

1968 ◽  
Vol 48 (1) ◽  
pp. 89-109
Author(s):  
ANN E. KAMMER
Keyword(s):  
Motor Neurons ◽  
Muscle Activity ◽  
Motor Units ◽  
Wingbeat Frequency ◽  
Motor Patterns ◽  
Flight Pattern ◽  
Warm Up ◽  
Burst Length ◽  
Synergistic Muscles ◽  
Phase Relationships

1. The patterns of muscle activity during warm-up were compared to those of flight. In the skipper Hylephila phylaeus and in the hawk moths Celerio lineata and Mimas tiliae the intervals between bursts of muscle potentials are the same as the wingbeat periods of flight at the same thoracic temperature, and the burst length is the same as in flight. In saturniids the period and burst length are both shorter during wing-vibrating than during flight. 2. During wing-vibrating the amplitude of the wing movement is small, and some of the muscles which are antagonists in flight are active simultaneously. In Hylephila phylaeus and Celerio lineata there is a phase change between some synergistic muscles, while some antagonistic pairs retain the phase relationships of flight. During wing-vibrating in Mimas tiliae and in saturniids all the motor units sampled were active at the same time. 3. In M. tiliae a variety of phase relationships intermediate between those of wing-vibrating and flight were observed, including a case of ‘relative co-ordination’ between motor units in the mesothorax. The results exclude the possibility that a single pace-making centre drives the motor neurons in the flight pattern. 4. A model of the central nervous interactions which generate the observed motor patterns is proposed. It is postulated that a small group of positively coupled neurons produces bursts of impulses at the wingbeat frequency and that these groups interact to generate the phase relationships seen during warm-up and flight.

Motor organization in pharynx of Helix pomatia

1984 ◽  
Vol 52 (3) ◽  
pp. 389-409 ◽  
Author(s):  
M. Peters ◽  
U. Altrup
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Neuromuscular Junctions ◽  
Muscle Tension ◽  
Helix Pomatia ◽  
Single Motor ◽  
Cobalt Staining ◽  
Excitatory Junction Potentials ◽  
Individual Motor ◽  
Phase Relationships

Identified motor neurons in the buccal ganglia of Helix pomatia and pharynx muscles innervated by them were studied with intracellular recording and cobalt staining. Retrograde cobalt staining via the buccal nerves indicated that neurons occupy relatively constant positions within the ganglia. With intracellular cobalt staining it was shown that the shape of a representative motor neuron (B4) is similar in different preparations. In some cases, however, deviations from the normal pattern of axon distribution were found. Presumed motor endings of neuron B4 in the muscle were also visualized with intracellular staining. Recordings from individual motor neurons show typical phase relationships of spontaneous spike activity. Most motor neurons are active in the retraction phase of the radula. Only excitatory motor neurons were found. Most neurons directly supply more than one muscle. Amplitude of excitatory junction potentials (EJP) and plasticity at neuromuscular junctions from one neuron are similar in different muscles. Single muscle fibers receive polyneuronal innervation. Activity of single motor neurons already leads to muscle contraction even without spiking of the muscle cells. Muscle tension depends on integrated EJP size. Most motor neurons supply typical combinations of a set of muscles. Thus, several muscles can be activated synchronously by activity of a single motor neuron. In this way muscle combinations are predetermined morphologically by the peripheral branching patterns of the respective neurons.

scholarly journals Global transcriptome profile of the developmental principles of in vitro iPSC-to-motor neuron differentiation

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Emilia Solomon ◽  
Katie Davis-Anderson ◽  
Blake Hovde ◽  
Sofiya Micheva-Viteva ◽  
Jennifer Foster Harris ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Acetylcholine Receptors ◽  
Gene Networks ◽  
Spinal Cord Injuries ◽  
Regulatory Gene ◽  
Transcriptome Profile

Abstract Background Human induced pluripotent stem cells (iPSC) have opened new avenues for regenerative medicine. Consequently, iPSC-derived motor neurons have emerged as potentially viable therapies for spinal cord injuries and neurodegenerative disorders including Amyotrophic Lateral Sclerosis. However, direct clinical application of iPSC bears in itself the risk of tumorigenesis and other unforeseeable genetic or epigenetic abnormalities. Results Employing RNA-seq technology, we identified and characterized gene regulatory networks triggered by in vitro chemical reprogramming of iPSC into cells with the molecular features of motor neurons (MNs) whose function in vivo is to innervate effector organs. We present meta-transcriptome signatures of 5 cell types: iPSCs, neural stem cells, motor neuron progenitors, early motor neurons, and mature motor neurons. In strict response to the chemical stimuli, along the MN differentiation axis we observed temporal downregulation of tumor growth factor-β signaling pathway and consistent activation of sonic hedgehog, Wnt/β-catenin, and Notch signaling. Together with gene networks defining neuronal differentiation (neurogenin 2, microtubule-associated protein 2, Pax6, and neuropilin-1), we observed steady accumulation of motor neuron-specific regulatory genes, including Islet-1 and homeobox protein HB9. Interestingly, transcriptome profiling of the differentiation process showed that Ca2+ signaling through cAMP and LPC was downregulated during the conversion of the iPSC to neural stem cells and key regulatory gene activity of the pathway remained inhibited until later stages of motor neuron formation. Pathways shaping the neuronal development and function were well-represented in the early motor neuron cells including, neuroactive ligand-receptor interactions, axon guidance, and the cholinergic synapse formation. A notable hallmark of our in vitro motor neuron maturation in monoculture was the activation of genes encoding G-coupled muscarinic acetylcholine receptors and downregulation of the ionotropic nicotinic acetylcholine receptors expression. We observed the formation of functional neuronal networks as spontaneous oscillations in the extracellular action potentials recorded on multi-electrode array chip after 20 days of differentiation. Conclusions Detailed transcriptome profile of each developmental step from iPSC to motor neuron driven by chemical induction provides the guidelines to novel therapeutic approaches in the re-construction efforts of muscle innervation.

scholarly journals Lipidomics study of plasma from patients suggest that ALS and PLS are part of a continuum of motor neuron disorders

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Estela Area-Gomez ◽  
D. Larrea ◽  
T. Yun ◽  
Y. Xu ◽  
J. Hupf ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Cell Structure ◽  
Disease Onset ◽  
Point Of View ◽  
Motor Dysfunction ◽  
Cellular Processes ◽  
Progressive Muscle Weakness ◽  
Human Pathology ◽  
Lateral Sclerosis

AbstractMotor neuron disorders (MND) include a group of pathologies that affect upper and/or lower motor neurons. Among them, amyotrophic lateral sclerosis (ALS) is characterized by progressive muscle weakness, with fatal outcomes only in a few years after diagnosis. On the other hand, primary lateral sclerosis (PLS), a more benign form of MND that only affects upper motor neurons, results in life-long progressive motor dysfunction. Although the outcomes are quite different, ALS and PLS present with similar symptoms at disease onset, to the degree that both disorders could be considered part of a continuum. These similarities and the lack of reliable biomarkers often result in delays in accurate diagnosis and/or treatment. In the nervous system, lipids exert a wide variety of functions, including roles in cell structure, synaptic transmission, and multiple metabolic processes. Thus, the study of the absolute and relative concentrations of a subset of lipids in human pathology can shed light into these cellular processes and unravel alterations in one or more pathways. In here, we report the lipid composition of longitudinal plasma samples from ALS and PLS patients initially, and after 2 years following enrollment in a clinical study. Our analysis revealed common aspects of these pathologies suggesting that, from the lipidomics point of view, PLS and ALS behave as part of a continuum of motor neuron disorders.

scholarly journals Poor Corticospinal Motor Neuron Health Is Associated with Increased Symptom Severity in the Acute Phase Following Repetitive Mild TBI and Predicts Early ALS Onset in Genetically Predisposed Rodents

2021 ◽  
Vol 11 (2) ◽  
pp. 160
Author(s):  
Mor R. Alkaslasi ◽  
Noell E. Cho ◽  
Navpreet K. Dhillon ◽  
Oksana Shelest ◽  
Patricia S. Haro-Lopez ◽  
...  
Keyword(s):  
Risk Factor ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Disease Onset ◽  
Poor Health ◽  
Disease Symptoms ◽  
Established Risk Factor ◽  
Early Injury ◽  
Corticospinal Motor Neurons ◽  
Lateral Sclerosis

Traumatic brain injury (TBI) is a well-established risk factor for several neurodegenerative disorders including Alzheimer’s disease and Parkinson’s disease, however, a link between TBI and amyotrophic lateral sclerosis (ALS) has not been clearly elucidated. Using the SOD1G93A rat model known to recapitulate the human ALS condition, we found that exposure to mild, repetitive TBI lead ALS rats to experience earlier disease onset and shortened survival relative to their sham counterparts. Importantly, increased severity of early injury symptoms prior to the onset of ALS disease symptoms was linked to poor health of corticospinal motor neurons and predicted worsened outcome later in life. Whereas ALS rats with only mild behavioral injury deficits exhibited no observable changes in corticospinal motor neuron health and did not present with early onset or shortened survival, those with more severe injury-related deficits exhibited alterations in corticospinal motor neuron health and presented with significantly earlier onset and shortened lifespan. While these studies do not imply that TBI causes ALS, we provide experimental evidence that head injury is a risk factor for earlier disease onset in a genetically predisposed ALS population and is associated with poor health of corticospinal motor neurons.

scholarly journals Sensory and motor neuron-derived factor. A novel heregulin variant highly expressed in sensory and motor neurons.

1995 ◽  
Vol 270 (44) ◽  
pp. 26722
Author(s):  
Wei-Hsien Ho ◽  
Mark P. Armanini ◽  
Andrew Nuijens ◽  
Heidi S. Phillips ◽  
Phyllis L. Osheroff
Keyword(s):  
Motor Neuron ◽  
Motor Neurons

scholarly journals ALS-Like Disorder in Three HIV-Positive Patients: Case Series

2021 ◽  
pp. 59-64
Author(s):  
Zachary Aaron Satin ◽  
Elham Bayat
Keyword(s):  
Antiretroviral Therapy ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Motor Neurons ◽  
Case Series ◽  
Retrospective Chart Review ◽  
Effective Control ◽  
Hiv Positive ◽  
Disease Course ◽  
Retroviral Infection

There appears to be a relationship between retroviruses such as HIV and the development of an ALS-like syndrome. Few cases have been reported; however, there exists evidence of a higher frequency of motor neuron disease in HIV-infected patients, as well as potential slowing and reversibility of disease course with combination antiretroviral therapy. We conducted a retrospective chart review of patients presenting to the George Washington University ALS Clinic from September 2006 to June 2018 to identify patients with HIV receiving HAART who were subsequently diagnosed with ALS or an ALS-like disorder. Our goals were to describe our patients’ disease course and compare them to general characteristics of ALS. We report three cases of HIV-positive individuals, all male, who were subsequently diagnosed with ALS. Each presented with symptoms of limb onset ALS with involvement of upper and lower motor neurons and whose disease originated at the cervical level. All three had been diagnosed with HIV prior to presentation and were presumably compliant with antiretroviral therapy throughout. Our patients demonstrated effective control of their HIV infection. Each experienced relatively slow progression of motor impairment compared to general ALS characteristics. Our study offers a distinct profile of HIV-positive patients compliant with HAART subsequently diagnosed with an ALS-like disorder. Further study should aim to uncover pathophysiological similarities between motor neuron disease both in the presence and absence of retroviral infection and to develop effective medical therapy for each.

scholarly journals Mutant VAPB: Culprit or Innocent Bystander of Amyotrophic Lateral Sclerosis?

Contact ◽  
2021 ◽  
Vol 4 ◽  
pp. 251525642110225
Author(s):  
Nica Borgese ◽  
Francesca Navone ◽  
Nobuyuki Nukina ◽  
Tomoyuki Yamanaka
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Dominant Negative ◽  
Negative Effects ◽  
Membrane Contact Sites ◽  
Familial Form ◽  
Main Driver ◽  
Mechanistic Basis ◽  
Lateral Sclerosis

Nearly twenty years ago a mutation in the VAPB gene, resulting in a proline to serine substitution (p.P56S), was identified as the cause of a rare, slowly progressing, familial form of the motor neuron degenerative disease Amyotrophic Lateral Sclerosis (ALS). Since then, progress in unravelling the mechanistic basis of this mutation has proceeded in parallel with research on the VAP proteins and on their role in establishing membrane contact sites between the ER and other organelles. Analysis of the literature on cellular and animal models reviewed here supports the conclusion that P56S-VAPB, which is aggregation-prone, non-functional and unstable, is expressed at levels that are insufficient to support toxic gain-of-function or dominant negative effects within motor neurons. Instead, insufficient levels of the product of the single wild-type allele appear to be required for pathological effects, and may be the main driver of the disease. In light of the multiple interactions of the VAP proteins, we address the consequences of specific VAPB depletion and highlight various affected processes that could contribute to motor neuron degeneration. In the future, distinction of specific roles of each of the two VAP paralogues should help to further elucidate the basis of p.P56S familial ALS, as well as of other more common forms of the disease.

scholarly journals Skeletal Muscle Metabolism: Origin or Prognostic Factor for Amyotrophic Lateral Sclerosis (ALS) Development?

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1449
Author(s):  
Cyril Quessada ◽  
Alexandra Bouscary ◽  
Frédérique René ◽  
Cristiana Valle ◽  
Alberto Ferri ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Muscle Metabolism ◽  
The Body ◽  
Energy Deficit ◽  
Acid Oxidation ◽  
Progression Of Disease ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive and selective loss of motor neurons, amyotrophy and skeletal muscle paralysis usually leading to death due to respiratory failure. While generally considered an intrinsic motor neuron disease, data obtained in recent years, including our own, suggest that motor neuron protection is not sufficient to counter the disease. The dismantling of the neuromuscular junction is closely linked to chronic energy deficit found throughout the body. Metabolic (hypermetabolism and dyslipidemia) and mitochondrial alterations described in patients and murine models of ALS are associated with the development and progression of disease pathology and they appear long before motor neurons die. It is clear that these metabolic changes participate in the pathology of the disease. In this review, we summarize these changes seen throughout the course of the disease, and the subsequent impact of glucose–fatty acid oxidation imbalance on disease progression. We also highlight studies that show that correcting this loss of metabolic flexibility should now be considered a major goal for the treatment of ALS.

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