scholarly journals A genetic manipulation of motor neuron excitability does not alter locomotor output in Drosophila larvae

2015 ◽  
Author(s):  
Erin C. McKiernan
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Motor Behavior ◽  
Genetic Manipulation ◽  
Motor Output ◽  
Neuron Excitability ◽  
Motor Neuron Excitability ◽  
The Face ◽  
Neuron Function

Are motor neurons just passive relayers of the signals they receive? Or, do motor neurons shape the signals before passing them on to the muscles, thereby influencing the timing of motor behavior? Few direct tests of the role of motor neuron intrinsic properties in shaping motor behavior have been carried out, and many questions remain about the role of specific ion channel genes in motor neuron function. In this study, two potassium channel transgenes were expressed in Drosophila larval motor neurons to increase their excitability. Mosaic animals were created in which some identified motor neurons expressed the transgenes while others did not. Motor output underlying crawling was compared in muscles innervated by control and experimental neurons in the same animals. No effect of the transgenic manipulation on motor output was seen. Possible explanations for these results are discussed, and future experiments are outlined that could shed light on how the larval nervous system produces normal motor output in the face of altered motor neuron excitability.

scholarly journals A genetic manipulation of motor neuron excitability does not alter locomotor output in Drosophila larvae

2015 ◽  
Author(s):  
Erin C. McKiernan
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Motor Behavior ◽  
Genetic Manipulation ◽  
Motor Output ◽  
Neuron Excitability ◽  
Motor Neuron Excitability ◽  
The Face ◽  
Neuron Function

Are motor neurons just passive relayers of the signals they receive? Or, do motor neurons shape the signals before passing them on to the muscles, thereby influencing the timing of motor behavior? Few direct tests of the role of motor neuron intrinsic properties in shaping motor behavior have been carried out, and many questions remain about the role of specific ion channel genes in motor neuron function. In this study, two potassium channel transgenes were expressed in Drosophila larval motor neurons to increase their excitability. Mosaic animals were created in which some identified motor neurons expressed the transgenes while others did not. Motor output underlying crawling was compared in muscles innervated by control and experimental neurons in the same animals. No effect of the transgenic manipulation on motor output was seen. Possible explanations for these results are discussed, and future experiments are outlined that could shed light on how the larval nervous system produces normal motor output in the face of altered motor neuron excitability.

scholarly journals A genetic manipulation of motor neuron excitability does not alter locomotor output in Drosophila larvae

2015 ◽  
Author(s):  
Erin C. McKiernan
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Motor Behavior ◽  
Genetic Manipulation ◽  
Motor Output ◽  
Neuron Excitability ◽  
Motor Neuron Excitability ◽  
The Face ◽  
Neuron Function

Are motor neurons just passive relayers of the signals they receive? Or, do motor neurons shape the signals before passing them on to the muscles, thereby influencing the timing of motor behavior? Few direct tests of the role of motor neuron intrinsic properties in shaping motor behavior have been carried out, and many questions remain about the role of specific ion channel genes in motor neuron function. In this study, two potassium channel transgenes were expressed in Drosophila larval motor neurons to increase their excitability. Mosaic animals were created in which some identified motor neurons expressed the transgenes while others did not. Motor output underlying crawling was compared in muscles innervated by control and experimental neurons in the same animals. Counterintuitively, no effect of the transgenic manipulation on motor output was seen. Future experiments are outlined to determine how the larval nervous system produces normal motor output in the face of altered motor neuron excitability.

scholarly journals A genetic manipulation of motor neuron excitability does not alter locomotor output in Drosophila larvae

2014 ◽  
Author(s):  
Erin C. McKiernan
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Motor Behavior ◽  
Genetic Manipulation ◽  
Motor Output ◽  
Membrane Properties ◽  
Neuron Excitability ◽  
Motor Neuron Excitability ◽  
The Face

Motor activity, like that producing locomotion, is generated by networks of neurons. At the last output level of these networks are the motor neurons, which send signals to the muscles, causing them to contract. Current research in motor control is focused on finding out how motor neurons contribute to shaping the timing of motor behaviors. Are motor neurons just passive relayers of the signals they receive? Or, do motor neurons shape the signals before passing them on to the muscles, thereby influencing the timing of the behavior? It is now well accepted that motor neurons have active, intrinsic membrane properties - there are ion channels in the cell membrane that allow motor neurons to respond to input in non-linear and diverse ways. However, few direct tests of the role of motor neuron intrinsic properties in shaping motor behavior have been carried out, and many questions remain about the role of specific ion channel genes in motor neuron function. In this study, two potassium channel transgenes were expressed in Drosophila larvae, causing motor neurons to fire at lower levels of current stimulation and at higher frequencies, thereby increasing excitability. Mosaic animals were created in which some identified motor neurons expressed the transgenes while others did not. Motor output underlying crawling was compared in muscles innervated by control and experimental neurons in the same animals. Counterintuitively, no effect of the transgenic manipulation on motor output was seen. Future experiments are outlined to determine how the larval nervous system produces normal motor output in the face of altered motor neuron excitability.

scholarly journals The Drosophila melanogaster Translational Repressor Pumilio Regulates Neuronal Excitability

Genetics ◽  
2002 ◽  
Vol 161 (3) ◽  
pp. 1177-1185 ◽  
Author(s):  
Brett A Schweers ◽  
Karina J Walters ◽  
Michael Stern
Keyword(s):  
Nervous System ◽  
Motor Neuron ◽  
Neuronal Excitability ◽  
P Element ◽  
Female Sterility ◽  
Neuronal Hyperexcitability ◽  
Translational Repressor ◽  
Neuron Excitability ◽  
Motor Neuron Excitability

Abstract Maintenance of proper neuronal excitability is vital to nervous system function and normal behavior. A subset of Drosophila mutants that exhibit altered behavior also exhibit defective motor neuron excitability, which can be monitored with electrophysiological methods. One such mutant is the P-element insertion mutant bemused (bem). The bem mutant exhibits female sterility, sluggishness, and increased motor neuron excitability. The bem P element is located in the large intron of the previously characterized translational repressor gene pumilio (pum). Here, by several criteria, we show that bem is a new allele of pum. First, ovary-specific expression of pum partially rescues bem female sterility. Second, pum null mutations fail to complement bem female sterility, behavioral defects, and neuronal hyperexcitability. Third, heads from bem mutant flies exhibit greatly reduced levels of Pum protein and the absence of two pum transcripts. Fourth, two previously identified pum mutants exhibit neuronal hyperexcitability. Fifth, overexpression of pum in the nervous system reduces neuronal excitability, which is the opposite phenotype to pum loss of function. Collectively, these findings describe a new role of pum in the regulation of neuronal excitability and may afford the opportunity to study the role of translational regulation in the maintenance of proper neuronal excitability.

scholarly journals Omega-3 Hastens and Omega-6 Delays the Progression of Neuropathology in a Murine Model of Familial ALS

2017 ◽  
Vol 11 (1) ◽  
pp. 84-91 ◽  
Author(s):  
Edward F. Boumil ◽  
Rishel Brenna Vohnoutka ◽  
Yuguan Liu ◽  
Sangmook Lee ◽  
Thomas B Shea
Keyword(s):  
Quality Of Life ◽  
Motor Neuron ◽  
Motor Function ◽  
Motor Neurons ◽  
Omega 3 ◽  
Self Medication ◽  
Familial Als ◽  
Neuron Function ◽  
The Impact

Background: Amyotrophic lateral sclerosis (ALS) is a progressive disease of motor neurons that has no cure or effective treatment. Any approach that could sustain minor motor function during terminal stages would improve quality of life. Objective: We examined the impact of omega-3 (Ω-3) and Ω-6, on motor neuron function in mice expressing mutant human superoxide dismutase-1 (SOD-1), which dominantly confers familial ALS and induces a similar sequence of motor neuron decline and eventual death when expressed in mice. Method: Mice received standard diets supplemented with equivalent amounts of Ω-3 and Ω-6 or a 10x increase in Ω-6 with no change in Ω-3 commencing at 4 weeks of age. Motor function and biochemical/histological parameters were assayed by standard methodologies. Results: Supplementation with equivalent Ω-3 and Ω-6 hastened motor neuron pathology and death, while 10x Ω-6 with no change in Ω-3 significantly delayed motor neuron pathology, including preservation of minor motor neuron function during the terminal stage. Conclusion: In the absence of a cure or treatment, affected individuals may resort to popular nutritional supplements such as Ω-3 as a form of “self-medication”. However, our findings and those of other laboratories indicate that such an approach could be harmful. Our findings suggest that a critical balance of Ω-6 and Ω-3 may temporarily preserve motor neuron function during the terminal stages of ALS, which could provide a substantial improvement in quality of life for affected individuals and their caregivers.

scholarly journals Gamma motor neurons survive and exacerbate alpha motor neuron degeneration in ALS

2016 ◽  
Vol 113 (51) ◽  
pp. E8316-E8325 ◽  
Author(s):  
Melanie Lalancette-Hebert ◽  
Aarti Sharma ◽  
Alexander K. Lyashchenko ◽  
Neil A. Shneider
Keyword(s):  
Motor Neuron ◽  
Mouse Models ◽  
Motor Neurons ◽  
Muscle Spindles ◽  
Excitatory Input ◽  
Synaptic Excitation ◽  
Fused In Sarcoma ◽  
Alpha Motor Neuron ◽  
Lateral Sclerosis

The molecular and cellular basis of selective motor neuron (MN) vulnerability in amyotrophic lateral sclerosis (ALS) is not known. In genetically distinct mouse models of familial ALS expressing mutant superoxide dismutase-1 (SOD1), TAR DNA-binding protein 43 (TDP-43), and fused in sarcoma (FUS), we demonstrate selective degeneration of alpha MNs (α-MNs) and complete sparing of gamma MNs (γ-MNs), which selectively innervate muscle spindles. Resistant γ-MNs are distinct from vulnerable α-MNs in that they lack synaptic contacts from primary afferent (IA) fibers. Elimination of these synapses protects α-MNs in the SOD1 mutant, implicating this excitatory input in MN degeneration. Moreover, reduced IAactivation by targeted reduction of γ-MNs in SOD1G93Amutants delays symptom onset and prolongs lifespan, demonstrating a pathogenic role of surviving γ-MNs in ALS. This study establishes the resistance of γ-MNs as a general feature of ALS mouse models and demonstrates that synaptic excitation of MNs within a complex circuit is an important determinant of relative vulnerability in ALS.

The control of rostrocaudal pattern in the developing spinal cord: specification of motor neuron subtype identity is initiated by signals from paraxial mesoderm

Development ◽  
1998 ◽  
Vol 125 (6) ◽  
pp. 969-982 ◽  
Author(s):  
M. Ensini ◽  
T.N. Tsuchida ◽  
H.G. Belting ◽  
T.M. Jessell
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Neural Tube ◽  
Motor Behavior ◽  
Neural Tube Closure ◽  
Paraxial Mesoderm ◽  
Homeodomain Protein ◽  
Mesodermal Cell ◽  
Developing Spinal Cord

The generation of distinct classes of motor neurons is an early step in the control of vertebrate motor behavior. To study the interactions that control the generation of motor neuron subclasses in the developing avian spinal cord we performed in vivo grafting studies in which either the neural tube or flanking mesoderm were displaced between thoracic and brachial levels. The positional identity of neural tube cells and motor neuron subtype identity was assessed by Hox and LIM homeodomain protein expression. Our results show that the rostrocaudal identity of neural cells is plastic at the time of neural tube closure and is sensitive to positionally restricted signals from the paraxial mesoderm. Such paraxial mesodermal signals appear to control the rostrocaudal identity of neural tube cells and the columnar subtype identity of motor neurons. These results suggest that the generation of motor neuron subtypes in the developing spinal cord involves the integration of distinct rostrocaudal and dorsoventral patterning signals that derive, respectively, from paraxial and axial mesodermal cell groups.

Sign in / Sign up

Export Citation Format

Share Document