scholarly journals Superoxide-imbalance pharmacologically induced by Rotenone triggers behavioral, neural, and inflammatory alterations in the Eisenia fetida earthworm

2021 ◽  
Author(s):  
Moisés Henrique Mastella ◽  
Isabel Roggia ◽  
Bárbara Osmarin Turra ◽  
Cibele Ferreira Teixeira ◽  
Charles Elias Assmann ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Eisenia Fetida ◽  
Body Wall ◽  
Escape Behavior ◽  
Receptor Gene ◽  
The Body ◽  
Stressful Events ◽  
Experimental Investigations ◽  
Mitochondrial Superoxide ◽  
Acetylcholine Receptor Gene

Abstract Background: The inflammatory theory of depression has been tested from epidemiological and experimental investigations. Some studies have suggested that mitochondrial dysfunction superoxide imbalance could increase the susceptibility to chronic stressful events, contributing to the establishment of chronic inflammation and the development of mood disorders. If this premise is true, mitochondrial superoxide imbalance induced by some molecules, such as Rotenone could be evolutionary conservated causing behavioral, immune, and neurological alterations in animals with the primitive central nervous system. Objective: To test this hypothesis, we analyzed some behavioral, immune, and histological markers in Eisenia fetida earthworms chronically exposed to Rotenone, that causes mitochondrial impairment for 14 days. Methods: earthworms were put in an artificial soil containing 30 nM of Rotenone distributed into a plastic cup that allowed the earthworms to leave and return freely into the ground. Since these organisms prefer to be buried in the ground, the model predicted that the earthworm would necessarily have to return to the Rotenone-contaminated medium creating a stressful condition. The effect on survival behavior, in the immune and histological body wall and ventral nervous ganglia (VNG) structures were evaluated, as well gene expression related to inflammation, mitochondrial and neuromuscular changes. Results: Rotenone-induced loss of earthworm escape behavior triggered by boric acid presence; it caused immune alterations indicatives of chronic inflammatory states. Some histological changes in the body wall and VNG indicated a possible earthworm reaction aimed at protection against Rotenone. Overexpression of the nicotinic acetylcholine receptor gene (nAChRs α5) in neural tissues could also help earthworms to reduce the degenerative impact of Rotenone on dopaminergic neurons. Conclusion: The data suggest that mitochondrial dysfunction could be an evolutionarily conserved element in inducing inflammatory and behavioral changes related to exposure to chronic stress.

Fictive locomotion induced by octopamine in the earthworm

2002 ◽  
Vol 205 (2) ◽  
pp. 265-271
Author(s):  
Kenji Mizutani ◽  
Hiroto Ogawa ◽  
Junichi Saito ◽  
Kotaro Oka
Keyword(s):  
Propagation Velocity ◽  
Eisenia Fetida ◽  
Body Wall ◽  
Motor Pattern ◽  
The Body ◽  
Neuron Activity ◽  
Fictive Locomotion ◽  
Burst Frequency ◽  
Motor Patterns ◽  
Bath Application

SUMMARY We investigated the function of octopamine (OA) as a motor pattern inducer in the earthworm Eisenia fetida. We used semi-intact preparations, consisting of 20 sequential segmental ganglia of the ventral nerve cord (VNC) together with the body wall from the middle of the animal. Bath-application of 10–4 mol l–1 OA to the semi-intact preparation induced phasic muscle contractions, which are consistent with crawling. In the isolated VNC, OA induced bursts of motor neuron activity in the first lateral nerves. Burst frequency increased with OA concentration, with a large increase in activity observed in the range 10–6–10–4 mol l–1. At 10–4 mol l–1, the coefficient of variation of burst periods (BPs) was smaller than that seen upon application of OA at other concentrations, which is indicative of rhythmic bursts. These rhythmic bursts propagated along the VNC from the anterior to posterior, with a propagation velocity ranging from 60 to 110 mm s–1. This velocity is consistent with the propagation velocity of muscle contraction during crawling behavior in the intact earthworm. From these results, we conclude that fictive crawling motor patterns are observed at 10–4 mol l–1 OA, and that OA can induce rhythmic bursts in the isolated VNC of the earthworm.

Lymphangiomatosis of the Body Wall: A Report of Two Cases Associated with Chylothorax and Fatal Outcome

1997 ◽  
Vol 17 (4) ◽  
pp. 617-624 ◽  
Author(s):  
Philippe Moerman ◽  
Chris Van Geet ◽  
Hugo Devlieger
Keyword(s):  
Body Wall ◽  
Fatal Outcome ◽  
The Body

scholarly journals A screen for genetic loci required for body-wall muscle development during embryogenesis in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 137 (2) ◽  
pp. 483-498
Author(s):  
J Ahnn ◽  
A Fire
Keyword(s):  
Caenorhabditis Elegans ◽  
Myosin Heavy Chain ◽  
Muscle Cell ◽  
Heavy Chain ◽  
Body Wall ◽  
Muscle Development ◽  
Contractile Function ◽  
The Body ◽  
Body Wall Muscle ◽  
Genetic Loci

Abstract We have used available chromosomal deficiencies to screen for genetic loci whose zygotic expression is required for formation of body-wall muscle cells during embryogenesis in Caenorhabditis elegans. To test for muscle cell differentiation we have assayed for both contractile function and the expression of muscle-specific structural proteins. Monoclonal antibodies directed against two myosin heavy chain isoforms, the products of the unc-54 and myo-3 genes, were used to detect body-wall muscle differentiation. We have screened 77 deficiencies, covering approximately 72% of the genome. Deficiency homozygotes in most cases stain with antibodies to the body-wall muscle myosins and in many cases muscle contractile function is observed. We have identified two regions showing distinct defects in myosin heavy chain gene expression. Embryos homozygous for deficiencies removing the left tip of chromosome V fail to accumulate the myo-3 and unc-54 products, but express antigens characteristic of hypodermal, pharyngeal and neural development. Embryos lacking a large region on chromosome III accumulate the unc-54 product but not the myo-3 product. We conclude that there exist only a small number of loci whose zygotic expression is uniquely required for adoption of a muscle cell fate.

scholarly journals Cloning and sequencing of cDNA of Sarcophaga peregrina humoral lectin induced on injury of the body wall.

1985 ◽  
Vol 260 (22) ◽  
pp. 12228-12233 ◽  
Author(s):  
H Takahashi ◽  
H Komano ◽  
N Kawaguchi ◽  
N Kitamura ◽  
S Nakanishi ◽  
...  
Keyword(s):  
Body Wall ◽  
The Body ◽  
Cloning And Sequencing

scholarly journals Mutations Affecting Nerve Attachment of Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1611-1622 ◽  
Author(s):  
Go Shioi ◽  
Michinari Shoji ◽  
Masashi Nakamura ◽  
Takeshi Ishihara ◽  
Isao Katsura ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Body Wall ◽  
The Body ◽  
Genetic Loci ◽  
Muscle Attachment ◽  
C Elegans ◽  
Ventral Cord ◽  
Excretory Canal

Abstract Using a pan-neuronal GFP marker, a morphological screen was performed to detect Caenorhabditis elegans larval lethal mutants with severely disorganized major nerve cords. We recovered and characterized 21 mutants that displayed displacement or detachment of the ventral nerve cord from the body wall (Ven: ventral cord abnormal). Six mutations defined three novel genetic loci: ven-1, ven-2, and ven-3. Fifteen mutations proved to be alleles of previously identified muscle attachment/positioning genes, mup-4, mua-1, mua-5, and mua-6. All the mutants also displayed muscle attachment/positioning defects characteristic of mua/mup mutants. The pan-neuronal GFP marker also revealed that mutants of other mua/mup loci, such as mup-1, mup-2, and mua-2, exhibited the Ven defect. The hypodermis, the excretory canal, and the gonad were morphologically abnormal in some of the mutants. The pleiotropic nature of the defects indicates that ven and mua/mup genes are required generally for the maintenance of attachment of tissues to the body wall in C. elegans.

scholarly journals Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 588
Author(s):  
Hayden W. Hyatt ◽  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Chronic Diseases ◽  
Muscle Mass ◽  
Cancer Chemotherapy ◽  
Muscle Wasting ◽  
The Body ◽  
Common Denominator ◽  
Skeletal Muscle Wasting ◽  
Vital Functions

Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

The cuticle of adultNippostrongylus brasiliensis

Parasitology ◽  
1965 ◽  
Vol 55 (1) ◽  
pp. 173-181 ◽  
Author(s):  
D. L. Lee
Keyword(s):  
Electron Microscope ◽  
Body Wall ◽  
Technical Assistance ◽  
Cortical Layer ◽  
The Body ◽  
Collagen Fibrils ◽  
Intestinal Cells ◽  
Nippostrongylus Brasiliensis ◽  
Normal Appearance

The cuticle of adults ofNippostrongylus brasiliensishas been described using histological, histochemical and ultrastructural techniques.The cuticle has the following layers: an outer triple-layered membrane; a single cortical layer; a fluid-filled layer which is traversed by numerous collagen fibrils; struts which support the fourteen longitudinal ridges of the cuticle and which are suspended by collagen fibrils in the fluid-filled layer; two fibre layers, each layer apparently containing three layers of fibres; and a basement lamella.The fluid-filled layer contains haemoglobin and esterase.The muscles of the body wall are attached to either the basement lamella or to the fibre layers of the cuticle.The mitochondria of the hypodermis are of normal appearance.The longitudinal ridges of the cuticle appear to abrade the microvilli of the intestinal cells of the host.Possible functions of the cuticle are discussed.I wish to thank Dr P. Tate, in whose department this work was done, for helpful suggestions and criticism at all stages of this work, and Mr A. Page for technical assistance. I also wish to thank Professor Boyd for permission to use the electron microscope in the Department of Anatomy.

Lymphangiomatosis of the Body Wall: A Report of Two Cases Associated with Chylothorax and Fatal Outcome

1997 ◽  
Vol 17 (4) ◽  
pp. 617-624 ◽  
Author(s):  
Philippe Moerman ◽  
Chris Van Geet ◽  
Hugo Devlieger
Keyword(s):  
Body Wall ◽  
Fatal Outcome ◽  
The Body
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