scholarly journals Quantum dots exposure alters both development and function of D-type GABAergic motor neurons in nematode Caenorhabditis elegans

2015 ◽  
Vol 4 (2) ◽  
pp. 399-408 ◽  
Author(s):  
Yunli Zhao ◽  
Xiong Wang ◽  
Qiuli Wu ◽  
Yiping Li ◽  
Meng Tang ◽  
...  
Keyword(s):  
Quantum Dots ◽  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Nematode Caenorhabditis Elegans ◽  
Cdte Qds ◽  
And Function

Both translocation into targeted neurons and developmental and functional alterations in targeted neurons contribute to CdTe QDs neurotoxicity.

MPA-capped CdTe quantum dots exposure causes neurotoxic effects in nematode Caenorhabditis elegans by affecting the transporters and receptors of glutamate, serotonin and dopamine at the genetic level, or by increasing ROS, or both

Nanoscale ◽  
2015 ◽  
Vol 7 (48) ◽  
pp. 20460-20473 ◽  
Author(s):  
Tianshu Wu ◽  
Keyu He ◽  
Qinglin Zhan ◽  
Shengjun Ang ◽  
Jiali Ying ◽  
...  
Keyword(s):  
Quantum Dots ◽  
Caenorhabditis Elegans ◽  
Biomedical Applications ◽  
Biological Properties ◽  
Cdte Quantum Dots ◽  
Nematode Caenorhabditis Elegans ◽  
Neurotoxic Effects ◽  
Genetic Level

As quantum dots (QDs) are widely used in biomedical applications, the number of studies focusing on their biological properties is increasing.

scholarly journals Biological effects, translocation, and metabolism of quantum dots in the nematode Caenorhabditis elegans

2016 ◽  
Vol 5 (4) ◽  
pp. 1003-1011 ◽  
Author(s):  
Dayong Wang
Keyword(s):  
Quantum Dots ◽  
Caenorhabditis Elegans ◽  
Recent Progress ◽  
Biological Effects ◽  
Assay System ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans

We summarize recent progress on the biological effects, translocation, and metabolism of QDs in thein vivoassay system ofC. elegans.

scholarly journals Insulin signaling regulates the toxicity of traffic-related PM2.5 on intestinal development and function in nematode Caenorhabditis elegans

2015 ◽  
Vol 4 (2) ◽  
pp. 333-343 ◽  
Author(s):  
Ruilong Yang ◽  
Yunli Zhao ◽  
Xiaoming Yu ◽  
Zhiqing Lin ◽  
Zhuge Xi ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Molecular Basis ◽  
Insulin Signaling Pathway ◽  
Intestinal Development ◽  
Nematode Caenorhabditis Elegans ◽  
And Function

Insulin signaling pathway may act as an important molecular basis for the toxicity of traffic-related PM2.5 in Caenorhabditis elegans, a non-mammalian toxicological model.

Cell interactions control the direction of outgrowth, branching and fasciculation of the HSN axons of Caenorhabditis elegans

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 1071-1087 ◽  
Author(s):  
G. Garriga ◽  
C. Desai ◽  
H.R. Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Epithelial Cells ◽  
Motor Neurons ◽  
Growth Cone ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Egg Laying ◽  
Axonal Guidance ◽  
Nematode Caenorhabditis Elegans ◽  
Vulval Precursor Cells

The two serotonergic HSN motor neurons of the nematode Caenorhabditis elegans innervate the vulval muscles and stimulate egg laying by hermaphrodites. By analyzing mutant and laser-operated animals, we find that both epithelial cells of the developing vulva and axons of the ventral nerve cord are required for HSN axonal guidance. Vulval precursor cells help guide the growth cone of the emerging HSN axon to the ventral nerve cord. Vulval cells also cause the two HSN axons to join the ventral nerve cord in two separate fascicles and to defasciculate from the ventral nerve cord and branch at the vulva. The axons of either the PVP or PVQ neurons are also necessary for the HSN axons to run in two separate fascicles within the ventral nerve cord. Our observations indicate that the outgrowth of the HSN axon is controlled in multiple ways by both neuronal and nonneuronal cells.

scholarly journals Recognition of familiar food activates feeding via an endocrine serotonin signal in Caenorhabditis elegans

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Bo-mi Song ◽  
Serge Faumont ◽  
Shawn Lockery ◽  
Leon Avery
Keyword(s):  
Caenorhabditis Elegans ◽  
Food Intake ◽  
Motor Neurons ◽  
Serotonin Receptor ◽  
Behavioral Plasticity ◽  
Serotonin Release ◽  
Feeding Response ◽  
Nematode Caenorhabditis Elegans ◽  
Novel Bacteria ◽  
Insight Into

Familiarity discrimination has a significant impact on the pattern of food intake across species. However, the mechanism by which the recognition memory controls feeding is unclear. Here, we show that the nematode Caenorhabditis elegans forms a memory of particular foods after experience and displays behavioral plasticity, increasing the feeding response when they subsequently recognize the familiar food. We found that recognition of familiar food activates the pair of ADF chemosensory neurons, which subsequently increase serotonin release. The released serotonin activates the feeding response mainly by acting humorally and directly activates SER-7, a type 7 serotonin receptor, in MC motor neurons in the feeding organ. Our data suggest that worms sense the taste and/or smell of novel bacteria, which overrides the stimulatory effect of familiar bacteria on feeding by suppressing the activity of ADF or its upstream neurons. Our study provides insight into the mechanism by which familiarity discrimination alters behavior.

Expression of the unc-4 homeoprotein in Caenorhabditis elegans motor neurons specifies presynaptic input

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 2877-2886 ◽  
Author(s):  
D.M. Miller ◽  
C.J. Niemeyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Motor Neurons ◽  
Ventral Nerve Cord ◽  
Chimeric Protein ◽  
Precursor Cell ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Common Precursor ◽  
Post Synaptic Neuron ◽  
Beta Galactosidase

In the nematode, Caenorhabditis elegans, VA and VB motor neurons arise from a common precursor cell but adopt different morphologies and synapse with separate sets of interneurons in the ventral nerve cord. A mutation that inactivates the unc-4 homeodomain gene causes VA motor neurons to assume the VB pattern of synaptic input while retaining normal axonal polarity and output; the disconnection of VA motor neurons from their usual presynaptic partners blocks backward locomotion. We show that expression of a functional unc-4-beta-galactosidase chimeric protein in VA motor neurons restores wild-type movement to an unc-4 mutant. We propose that unc-4 controls a differentiated characteristic of the VA motor neurons that distinguishes them from their VB sisters, thus dictating recognition by the appropriate interneurons. Our results show that synaptic choice can be controlled at the level of transcription in the post-synaptic neuron and identify a homeoprotein that defines a subset of cell-specific traits required for this choice.

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