Understanding Diabetic Polyneuropathy and Longevity: What Can We Learn from the Nematode Caenorhabditis Elegans?

2012 ◽  
Vol 120 (04) ◽  
pp. 182-183 ◽  
Author(s):  
M. Mendler ◽  
A. Schlotterer ◽  
M. Morcos ◽  
P. Nawroth
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Neuronal Damage ◽  
Insulin Signalling ◽  
Diabetic Polyneuropathy ◽  
Nematode Caenorhabditis Elegans ◽  
Ideal Model ◽  
Complex Interplay ◽  
Intrinsic Factors ◽  
System A

AbstractPathogenesis of late diabetic complications is influenced by a complex interplay of multiple exogenous and intrinsic factors. The well characterised nematode Caenorhabditis elegans is an ideal model to study causes of diabetic polyneuropathy because of its easily accessible nervous system. A repertoire of methods allows the assessment of both morphological and functional glucotoxic damages as well as reduction of lifespan, thereby helping to examine the influence of different pathways and mechanisms on neurodegeneration. Its insulin signalling system allows to directly visualize effects of insulin on high glucose induced neuronal damage, leading to a better understanding of diabetic polyneuropathy.

Neuronal damage induced by nanopolystyrene particles in nematode Caenorhabditis elegans

2019 ◽  
Vol 6 (8) ◽  
pp. 2591-2601 ◽  
Author(s):  
Man Qu ◽  
Yan Kong ◽  
Yujie Yuan ◽  
Dayong Wang
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Neuronal Damage ◽  
Nematode Caenorhabditis Elegans

Our observations highlight the potential of nanoplastics in inducing damage on both development and functions of nervous system after long-term exposure.

scholarly journals Effects of NAD+ in Caenorhabditis elegans Models of Neuronal Damage

Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 993
Author(s):  
Yuri Lee ◽  
Hyeseon Jeong ◽  
Kyung Hwan Park ◽  
Kyung Won Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Therapeutic Strategy ◽  
Axon Regeneration ◽  
Neuronal Damage ◽  
Biological Processes ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Neuronal Functions ◽  
Molecular Components

Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor that mediates numerous biological processes in all living cells. Multiple NAD+ biosynthetic enzymes and NAD+-consuming enzymes are involved in neuroprotection and axon regeneration. The nematode Caenorhabditis elegans has served as a model to study the neuronal role of NAD+ because many molecular components regulating NAD+ are highly conserved. This review focuses on recent findings using C. elegans models of neuronal damage pertaining to the neuronal functions of NAD+ and its precursors, including a neuroprotective role against excitotoxicity and axon degeneration as well as an inhibitory role in axon regeneration. The regulation of NAD+ levels could be a promising therapeutic strategy to counter many neurodegenerative diseases, as well as neurotoxin-induced and traumatic neuronal damage.

scholarly journals μ2 adaptin facilitates but is not essential for synaptic vesicle recycling in Caenorhabditis elegans

2008 ◽  
Vol 183 (5) ◽  
pp. 881-892 ◽  
Author(s):  
Mingyu Gu ◽  
Kim Schuske ◽  
Shigeki Watanabe ◽  
Qiang Liu ◽  
Paul Baum ◽  
...  
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Synaptic Vesicle ◽  
Synaptic Vesicles ◽  
Evoked Responses ◽  
Nematode Caenorhabditis Elegans ◽  
Synaptic Vesicle Recycling ◽  
Specific Loss ◽  
Vesicle Recycling ◽  
Cargo Proteins

Synaptic vesicles must be recycled to sustain neurotransmission, in large part via clathrin-mediated endocytosis. Clathrin is recruited to endocytic sites on the plasma membrane by the AP2 adaptor complex. The medium subunit (μ2) of AP2 binds to cargo proteins and phosphatidylinositol-4,5-bisphosphate on the cell surface. Here, we characterize the apm-2 gene (also called dpy-23), which encodes the only μ2 subunit in the nematode Caenorhabditis elegans. APM-2 is highly expressed in the nervous system and is localized to synapses; yet specific loss of APM-2 in neurons does not affect locomotion. In apm-2 mutants, clathrin is mislocalized at synapses, and synaptic vesicle numbers and evoked responses are reduced to 60 and 65%, respectively. Collectively, these data suggest AP2 μ2 facilitates but is not essential for synaptic vesicle recycling.

scholarly journals The beginning of connectomics: a commentary on White et al. (1986) ‘The structure of the nervous system of the nematode Caenorhabditis elegans ’

2015 ◽  
Vol 370 (1666) ◽  
pp. 20140309 ◽  
Author(s):  
Scott W. Emmons
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Synaptic Connections ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Synaptic Structure ◽  
Complete Set ◽  
The Mind ◽  
First Time ◽  
350Th Anniversary

The article ‘Structure of the nervous system of the nematode Caenorhabditis elegans ' (aka ‘The mind of a worm’) by White et al. , published for the first time the complete set of synaptic connections in the nervous system of an animal. The work was carried out as part of a programme to begin to understand how genes determine the structure of a nervous system and how a nervous system creates behaviour. It became a major stimulus to the field of C. elegans research, which has since contributed insights into all areas of biology. Twenty-six years elapsed before developments, notably more powerful computers, made new studies of this kind possible. It is hoped that one day knowledge of synaptic structure, the connectome , together with results of many other investigations, will lead to an understanding of the human brain. This commentary was written to celebrate the 350th anniversary of the journal Philosophical Transactions of the Royal Society .

scholarly journals Regulation of Microtubule Dynamics in Axon Regeneration: Insights from C. elegans

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 764 ◽  
Author(s):  
Ngang Heok Tang ◽  
Andrew D. Chisholm
Keyword(s):  
Caenorhabditis Elegans ◽  
Leucine Zipper ◽  
Axon Regeneration ◽  
Axonal Injury ◽  
External Environment ◽  
Nematode Caenorhabditis Elegans ◽  
Intrinsic Factors ◽  
C Elegans ◽  
And Control ◽  
Active Investigation

The capacity of an axon to regenerate is regulated by its external environment and by cell-intrinsic factors. Studies in a variety of organisms suggest that alterations in axonal microtubule (MT) dynamics have potent effects on axon regeneration. We review recent findings on the regulation of MT dynamics during axon regeneration, focusing on the nematode Caenorhabditis elegans. In C. elegans the dual leucine zipper kinase (DLK) promotes axon regeneration, whereas the exchange factor for Arf6 (EFA-6) inhibits axon regeneration. Both DLK and EFA-6 respond to injury and control axon regeneration in part via MT dynamics. How the DLK and EFA-6 pathways are related is a topic of active investigation, as is the mechanism by which EFA-6 responds to axonal injury. We evaluate potential candidates, such as the MT affinity-regulating kinase PAR-1/MARK, in regulation of EFA-6 and axonal MT dynamics in regeneration.

Optogenetic analyses of neuronal network function and synaptic transmission in Caenorhabditis elegans

e-Neuroforum ◽  
2014 ◽  
Vol 20 (4) ◽  
Author(s):  
A. Gottschalk
Keyword(s):  
Caenorhabditis Elegans ◽  
Optical Sensors ◽  
Behavioral Change ◽  
Nematode Caenorhabditis Elegans ◽  
Ideal Model ◽  
Network Function ◽  
Primary Signal ◽  
Ideal Model System ◽  
Chemical Synapses ◽  
Stimulation Of

AbstractThe transparent nematode Caenorhabditis elegans, with its anatomically well-defined nervous system comprising 302 neurons that regulate quantifiable behaviors, is an ideal model system for the development and ap­plication of optogenetic methods. Optoge­netically modified neurons can be acutely ex­cited or inhibited by light and the effects on a distinct behavior observed. Special light­ing systems allow the manipulation of several nerve cells that act as “nodes” of small neural circuits, with different colors of light, so as to control different optogenetic tools indepen­dently and simultaneously. In addition, ge­netically encoded optical sensors for neuro­nal activity make it possible to draw conclu­sions even when the optogenetic interven­tion causes no obvious behavioral change. The stimulation of quantifiable behaviors permits the analysis of the function of genes necessary in the corresponding neuron for the encoding or amplification of the primary signal. Finally, following optogenetic stimu­lation, the function of chemical synapses and their proteins can also be analyzed by elec­trophysiology or electron microscopy.

The structure of the nervous system of the nematode Caenorhabditis elegans

1986 ◽  
Vol 314 (1165) ◽  
pp. 1-340 ◽  
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Neuromuscular Junctions ◽  
Synaptic Connections ◽  
Serial Sections ◽  
Nematode Caenorhabditis Elegans ◽  
Invariant Structure ◽  
Parallel Processes ◽  
Total Complement ◽  
Chemical Synapses

The structure and connectivity of the nervous system of the nematode Caenorhabditis elegans has been deduced from reconstructions of electron micrographs of serial sections. The hermaphrodite nervous system has a total complement of 302 neurons, which are arranged in an essentially invariant structure. Neurons with similar morphologies and connectivities have been grouped together into classes; there are 118 such classes. Neurons have simple morphologies with few, if any, branches. Processes from neurons run in defined positions within bundles of parallel processes, synaptic connections being made en passant . Process bundles are arranged longitudinally and circumferentially and are often adjacent to ridges of hypodermis. Neurons are generally highly locally connected, making synaptic connections with many of their neighbours. Muscle cells have arms that run out to process bundles containing motoneuron axons. Here they receive their synaptic input in defined regions along the surface of the bundles, where motoneuron axons reside. Most of the m orphologically identifiable synaptic connections in a typical animal are described. These consist of about 5000 chemical synapses, 2000 neuromuscular junctions and 600 gap junctions.

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