scholarly journals PDF-1 neuropeptide signaling modulates a neural circuit for mate-searching behavior in C. elegans

2012 ◽  
Vol 15 (12) ◽  
pp. 1675-1682 ◽  
Author(s):  
Arantza Barrios ◽  
Rajarshi Ghosh ◽  
Chunhui Fang ◽  
Scott W Emmons ◽  
Maureen M Barr
Keyword(s):  
Neural Circuit ◽  
Searching Behavior ◽  
Mate Searching ◽  
C Elegans

scholarly journals Sensory Regulation of C. elegans Male Mate-Searching Behavior

2008 ◽  
Vol 18 (23) ◽  
pp. 1865-1871 ◽  
Author(s):  
Arantza Barrios ◽  
Stephen Nurrish ◽  
Scott W. Emmons
Keyword(s):  
Searching Behavior ◽  
Mate Searching ◽  
C Elegans ◽  
Sensory Regulation ◽  
Male Mate

scholarly journals Regulation ofCaenorhabditis elegansMale Mate Searching Behavior by the Nuclear Receptor DAF-12

Genetics ◽  
2008 ◽  
Vol 180 (4) ◽  
pp. 2111-2122 ◽  
Author(s):  
Gunnar Kleemann ◽  
Lingyun Jia ◽  
Scott W. Emmons
Keyword(s):  
Nuclear Receptor ◽  
Searching Behavior ◽  
Mate Searching

Live demonstration: Spiking neural circuit based navigation inspired by C. elegans thermotaxis

2015 ◽  
Author(s):  
Chirag Shetty ◽  
Sri Nitchith ◽  
Rishabh Rawat ◽  
S. R. Nandakumar ◽  
Pritesh Shah ◽  
...  
Keyword(s):  
Neural Circuit ◽  
C Elegans ◽  
Live Demonstration

scholarly journals Insulin-like signaling and the neural circuit for integrative behavior in C. elegans

2006 ◽  
Vol 20 (21) ◽  
pp. 2955-2960 ◽  
Author(s):  
E. Kodama ◽  
A. Kuhara ◽  
A. Mohri-Shiomi ◽  
K. D. Kimura ◽  
M. Okumura ◽  
...  
Keyword(s):  
Neural Circuit ◽  
C Elegans

A Dynamic Body Model of the NematodeC. eleganswith Neural Oscillators

2005 ◽  
Vol 17 (3) ◽  
pp. 318-326 ◽  
Author(s):  
Michiyo Suzuki ◽  
◽  
Takeshi Goto ◽  
Toshio Tsuji ◽  
Hisao Ohtake ◽  
...  
Keyword(s):  
Computer Simulation ◽  
Motor Control ◽  
Caenorhabditis Elegans ◽  
Neural Circuit ◽  
Rhythmic Movement ◽  
Circuit Model ◽  
Neural Oscillators ◽  
C Elegans ◽  
Body Model ◽  
Multicellular Organisms

The nematode <I>Caenorhabditis elegans (C. elegans)</I>, a relatively simple organism in structure, is one of the most well-studied multicellular organisms. We developed a <I>virtual C. elegans</I> based on the actual organism to analyze motor control. We propose a dynamic body model, including muscles, controlled by a neural circuit model based on the actual nematode. The model uses neural oscillators to generate rhythmic movement. Computer simulation confirmed that the <I>virtual C. elegans</I> realizes motor control similar qualitatively to that of the actual organism. Specified classes of neurons are killed in the neural circuit model corresponding to actual <I>unc</I> mutants, demonstrating that resulting movement of the <I>virtual C. elegans</I> resembles that of actual mutants.

scholarly journals Release-dependent feedback inhibition by a presynaptically localized ligand-gated anion channel

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Seika Takayanagi-Kiya ◽  
Keming Zhou ◽  
Yishi Jin
Keyword(s):  
Motor Neurons ◽  
Neurotransmitter Release ◽  
Neural Circuit ◽  
Feedback Inhibition ◽  
Release Kinetics ◽  
Anion Channel ◽  
C Elegans ◽  
Release Of Acetylcholine ◽  
Presynaptic Release

Presynaptic ligand-gated ion channels (LGICs) have long been proposed to affect neurotransmitter release and to tune the neural circuit activity. However, the understanding of their in vivo physiological action remains limited, partly due to the complexity in channel types and scarcity of genetic models. Here we report that C. elegans LGC-46, a member of the Cys-loop acetylcholine (ACh)-gated chloride (ACC) channel family, localizes to presynaptic terminals of cholinergic motor neurons and regulates synaptic vesicle (SV) release kinetics upon evoked release of acetylcholine. Loss of lgc-46 prolongs evoked release, without altering spontaneous activity. Conversely, a gain-of-function mutation of lgc-46 shortens evoked release to reduce synaptic transmission. This inhibition of presynaptic release requires the anion selectivity of LGC-46, and can ameliorate cholinergic over-excitation in a C. elegans model of excitation-inhibition imbalance. These data demonstrate a novel mechanism of presynaptic negative feedback in which an anion-selective LGIC acts as an auto-receptor to inhibit SV release.

scholarly journals RHO-1 and the Rho GEF RHGF-1 interact with UNC-6/Netrin signaling to regulate growth cone protrusion and microtubule organization in C. elegans

2019 ◽  
Author(s):  
Mahekta R. Gujar ◽  
Aubrie M. Stricker ◽  
Erik A. Lundquist
Keyword(s):  
Axon Guidance ◽  
Growth Cone ◽  
Neural Circuit ◽  
Growth Cones ◽  
Negative Regulator ◽  
Microtubule Organization ◽  
C Elegans ◽  
Guidance Cue ◽  
Rho Gef

AbstractUNC-6/Netrin is a conserved axon guidance cue that directs growth cone migrations in the dorsal-ventral axis of C. elegans and in the vertebrate spinal cord. UNC-6/Netrin is expressed in ventral cells, and growth cones migrate ventrally toward or dorsally away from UNC-6/Netrin. Recent studies of growth cone behavior during outgrowth in vivo in C. elegans have led to a polarity/protrusion model in directed growth cone migration away from UNC-6/Netrin. In this model, UNC-6/Netrin first polarizes the growth cone via the UNC-5 receptor, leading to dorsally biased protrusion and F-actin accumulation. UNC-6/Netrin then regulates protrusion based on this polarity. The receptor UNC-40/DCC drives protrusion dorsally, away from the UNC-6/Netrin source, and the UNC-5 receptor inhibits protrusion ventrally, near the UNC-6/Netrin source, resulting in dorsal migration. UNC-5 inhibits protrusion in part by excluding microtubules from the growth cone, which are pro-protrusive. Here we report that the RHO-1/RhoA GTPase and its activator GEF RHGF-1 inhibit growth cone protrusion and MT accumulation in growth cones, similar to UNC-5. However, growth cone polarity of protrusion and F-actin were unaffected by RHO-1 and RHGF-1. Thus, RHO-1 signaling acts specifically as a negative regulator of protrusion and MT accumulation, and not polarity. Genetic interactions suggest that RHO-1 and RHGF-1 act with UNC-5, as well as with a parallel pathway, to regulate protrusion. The cytoskeletal interacting molecule UNC-33/CRMP was required for RHO-1 activity to inhibit MT accumulation, suggesting that UNC-33/CRMP might act downstream of RHO-1. In sum, these studies describe a new role of RHO-1 and RHGF-1 in regulation of growth cone protrusion by UNC-6/Netrin.Author SummaryNeural circuits are formed by precise connections between axons. During axon formation, the growth cone leads the axon to its proper target in a process called axon guidance. Growth cone outgrowth involves asymmetric protrusion driven by extracellular cues that stimulate and inhibit protrusion. How guidance cues regulate growth cone protrusion in neural circuit formation is incompletely understood. This work shows that the signaling molecule RHO-1 acts downstream of the UNC-6/Netrin guidance cue to inhibit growth cone protrusion in part by excluding microtubules from the growth cone, which are structural elements that drive protrusion.

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