Characterization of the intracellularly recorded response of identified flight motor neurons inDrosophila

1983 ◽  
Vol 150 (3) ◽  
pp. 295-303 ◽  
Author(s):  
J. H. Koenig ◽  
Kazuo Ikeda
Keyword(s):  
Author(s):  
Jeffrey T. Bingham ◽  
Marco P. Schoen

Human muscle motion is initiated in the central nervous system where a nervous signal travels through the body and the motor neurons excite the muscles to move. These signals, termed myoelectric signals, can be measured on the surface of the skin as an electrical potential. By analyzing these signals it is possible to determine the muscle actions the signals elicit, and thus can be used in manipulating smart prostheses and teleoperation of machinery. Due to the randomness of myoelectric signals, identification of the signals is not complete, therefore the goal of this project is to complete a study of the characterization of one set of hand motions using current system identification methods. The gripping motion of the hand and the corresponding myoelectric signals are measured and the data captured with a personal computer. Using computer software the captured data are processed and finally subjected to several system identification routines. Using this technique it is possible to construct a mathematical model that correlates the myoelectric signals with the matching hand motion.


2001 ◽  
Vol 443 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Hiroyuki Konomi ◽  
Adrian C.B. Meedeniya ◽  
Maria E. Simula ◽  
James Toouli ◽  
Gino T.P. Saccone

2019 ◽  
Vol 28 (19) ◽  
pp. 3199-3210 ◽  
Author(s):  
Kevin A Kaifer ◽  
Eric Villalón ◽  
Benjamin S O'Brien ◽  
Samantha L Sison ◽  
Caley E Smith ◽  
...  

Abstract Spinal muscular atrophy (SMA) is a neuromuscular disease caused by deletions or mutations in survival motor neuron 1 (SMN1). The molecular mechanisms underlying motor neuron degeneration in SMA remain elusive, as global cellular dysfunction obscures the identification and characterization of disease-relevant pathways and potential therapeutic targets. Recent reports have implicated microRNA (miRNA) dysregulation as a potential contributor to the pathological mechanism in SMA. To characterize miRNAs that are differentially regulated in SMA, we profiled miRNA levels in SMA induced pluripotent stem cell (iPSC)-derived motor neurons. From this array, miR-23a downregulation was identified selectively in SMA motor neurons, consistent with previous reports where miR-23a functioned in neuroprotective and muscle atrophy-antagonizing roles. Reintroduction of miR-23a expression in SMA patient iPSC-derived motor neurons protected against degeneration, suggesting a potential miR-23a-specific disease-modifying effect. To assess this activity in vivo, miR-23a was expressed using a self-complementary adeno-associated virus serotype 9 (scAAV9) viral vector in the Smn2B/− SMA mouse model. scAAV9-miR-23a significantly reduced the pathology in SMA mice, including increased motor neuron size, reduced neuromuscular junction pathology, increased muscle fiber area, and extended survival. These experiments demonstrate that miR-23a is a novel protective modifier of SMA, warranting further characterization of miRNA dysfunction in SMA.


2018 ◽  
Vol 217 (9) ◽  
pp. 3127-3139 ◽  
Author(s):  
Xiu-Tang Cheng ◽  
Yu-Xiang Xie ◽  
Bing Zhou ◽  
Ning Huang ◽  
Tamar Farfel-Becker ◽  
...  

Despite widespread distribution of LAMP1 and the heterogeneous nature of LAMP1-labeled compartments, LAMP1 is routinely used as a lysosomal marker, and LAMP1-positive organelles are often referred to as lysosomes. In this study, we use immunoelectron microscopy and confocal imaging to provide quantitative analysis of LAMP1 distribution in various autophagic and endolysosomal organelles in neurons. Our study demonstrates that a significant portion of LAMP1-labeled organelles do not contain detectable lysosomal hydrolases including cathepsins D and B and glucocerebrosidase. A bovine serum albumin–gold pulse–chase assay followed by ultrastructural analysis suggests a heterogeneity of degradative capacity in LAMP1-labeled endolysosomal organelles. Gradient fractionation displays differential distribution patterns of LAMP1/2 and cathepsins D/B in neurons. We further reveal that LAMP1 intensity in familial amyotrophic lateral sclerosis–linked motor neurons does not necessarily reflect lysosomal deficits in vivo. Our study suggests that labeling a set of lysosomal hydrolases combined with various endolysosomal markers would be more accurate than simply relying on LAMP1/2 staining to assess neuronal lysosome distribution, trafficking, and functionality under physiological and pathological conditions.


2019 ◽  
Vol 31 (10) ◽  
Author(s):  
Adam Humenick ◽  
Bao Nan Chen ◽  
Chris I. W. Lauder ◽  
David A. Wattchow ◽  
Vladimir P. Zagorodnyuk ◽  
...  

1989 ◽  
Vol 279 (2) ◽  
pp. 272-280 ◽  
Author(s):  
S. Wang ◽  
R. M. Robertson

1995 ◽  
Vol 134 (1-2) ◽  
pp. 219-220
Author(s):  
Akiko Matsumoto ◽  
Hiide Yoshino ◽  
Nobuhiro Yuki ◽  
Yukichi Hara ◽  
Neil R. Cashman ◽  
...  

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