355 research outputs found

    Chemosensation: Tasting with the Tail

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    AbstractAnimals employ multiple mechanisms to detect the presence and location of environmental stimuli. Recent work suggests that Caenorhabditis elegans uses chemosensory information provided by spatially distinct sensilla to generate a sensory map of its environment and to avoid noxious compounds

    Sensorimotor Integration: Locating Locomotion in Neural Circuits

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    Neural components of the circuits that transform sensory cues into changes in motor activities are largely unknown. Several recent studies have now functionally mapped the sensorimotor circuits responsible for locomotion behaviors under defined environmental conditions in the nematode Caenorhabditis elegans

    Complement anaphylatoxin C5a neuroprotects through regulation of glutamate receptor subunit 2 in vitro and in vivo

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    <p>Abstract</p> <p>Background</p> <p>The complement system is thought to be involved in the pathogenesis of numerous neurological diseases. We previously reported that pre-treatment of murine cortico-hippocampal neuronal cultures with the complement derived anaphylatoxin C5a, protects against glutamate mediated apoptosis. Our present study with C5a receptor knock out (C5aRKO) mice corroborates that the deficiency of C5a renders C5aRKO mouse more susceptible to apoptotic injury <it>in vivo</it>. In this study we explored potential upstream mechanisms involved in C5a mediated neuroprotection <it>in vivo </it>and <it>in vitro</it>.</p> <p>Methods</p> <p>Based on evidence suggesting that reduced expression of glutamate receptor subunit 2 (GluR2) may influence apoptosis in neurons, we studied the effect of human recombinant C5a on GluR2 expression in response to glutamate neurotoxicity. Glutamate analogs were injected into C5aRKO mice or used to treat <it>in vitro </it>neuronal culture and GluR2 expression were assessed in respect with cell death.</p> <p>Results</p> <p>In C5aRKO mice we found that the neurons are more susceptible to excitotoxicity resulting in apoptotic injury in the absence of the C5a receptor compared to WT control mice. Our results suggest that C5a protects against apoptotic pathways in neurons <it>in vitro </it>and <it>in vivo </it>through regulation of GluR2 receptor expression.</p> <p>Conclusion</p> <p>Complement C5a neuroprotects through regulation of GluR2 receptor subunit.</p

    Regulation of Response Properties and Operating Range of the AFD Thermosensory Neurons by cGMP Signaling

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    SummaryBackgroundThe neuronal mechanisms that encode specific stimulus features in order to elicit defined behavioral responses are poorly understood. C. elegans forms a memory of its cultivation temperature (Tc) and exhibits distinct behaviors in different temperature ranges relative to Tc. In particular, C. elegans tracks isotherms only in a narrow temperature band near Tc. Tc memory is in part encoded by the threshold of responsiveness (T∗AFD) of the AFD thermosensory neuron pair to temperature stimuli. However, because AFD thermosensory responses appear to be similar at all examined temperatures above T∗AFD, the mechanisms that generate specific behaviors in defined temperature ranges remain to be determined.ResultsHere, we show that the AFD neurons respond to the sinusoidal variations in thermal stimuli followed by animals during isothermal tracking (IT) behavior only in a narrow temperature range near Tc. We find that mutations in the AFD-expressed gcy-8 receptor guanylyl cyclase (rGC) gene result in defects in the execution of IT behavior and are associated with defects in the responses of the AFD neurons to oscillating thermal stimuli. In contrast, mutations in the gcy-18 or gcy-23 rGCs alter the temperature range in which IT behavior is exhibited. Alteration of intracellular cGMP levels via rGC mutations or addition of cGMP analogs shift the lower and upper ranges of the temperature range of IT behavior in part via alteration in T∗AFD.ConclusionsOur observations provide insights into the mechanisms by which a single sensory neuron type encodes features of a given stimulus to generate different behaviors in defined zones

    Developmental programming modulates olfactory behavior in C. elegans via endogenous RNAi pathways

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    Environmental stress during early development can impact adult phenotypes via programmed changes in gene expression. C. elegans larvae respond to environmental stress by entering the stress-resistant dauer diapause pathway and resume development once conditions improve (postdauers). Here we show that the osm-9 TRPV channel gene is a target of developmental programming and is down-regulated specifically in the ADL chemosensory neurons of postdauer adults, resulting in a corresponding altered olfactory behavior that is mediated by ADL in an OSM-9-dependent manner. We identify a cis-acting motif bound by the DAF-3 SMAD and ZFP-1 (AF10) proteins that is necessary for the differential regulation of osm-9, and demonstrate that both chromatin remodeling and endo-siRNA pathways are major contributors to the transcriptional silencing of the osm-9 locus. This work describes an elegant mechanism by which developmental experience influences adult phenotypes by establishing and maintaining transcriptional changes via RNAi and chromatin remodeling pathways.1

    Feeding state-dependent regulation of developmental plasticity via CaMKI and neuroendocrine signaling

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    Information about nutrient availability is assessed via largely unknown mechanisms to drive developmental decisions, including the choice of Caenorhabditis elegans larvae to enter into the reproductive cycle or the dauer stage. In this study, we show that CMK-1 CaMKI regulates the dauer decision as a function of feeding state. CMK-1 acts cell-autonomously in the ASI, and non cell-autonomously in the AWC, sensory neurons to regulate expression of the growth promoting daf-7 TGF-β and daf-28 insulin-like peptide (ILP) genes, respectively. Feeding state regulates dynamic subcellular localization of CMK-1, and CMK-1-dependent expression of anti-dauer ILP genes, in AWC. A food-regulated balance between anti-dauer ILP signals from AWC and pro-dauer signals regulates neuroendocrine signaling and dauer entry; disruption of this balance in cmk-1 mutants drives inappropriate dauer formation under well-fed conditions. These results identify mechanisms by which nutrient information is integrated in a small neuronal network to modulate neuroendocrine signaling and developmental plasticity. © Neal et al.1

    A Forward Genetic Screen for Molecules Involved in Pheromone-Induced Dauer Formation in Caenorhabditis elegans

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    Animals must constantly assess their surroundings and integrate sensory cues to make appropriate behavioral and developmental decisions. Pheromones produced by conspecific individuals provide critical information regarding environmental conditions. Ascaroside pheromone concentration and composition are instructive in the decision of Caenorhabditis elegans to either develop into a reproductive adult or enter into the stress-resistant alternate dauer developmental stage. Pheromones are sensed by a small set of sensory neurons, and integrated with additional environmental cues, to regulate neuroendocrine signaling and dauer formation. To identify molecules required for pheromone-induced dauer formation, we performed an unbiased forward genetic screen and identified phd (pheromone response-defective dauer) mutants. Here, we describe new roles in dauer formation for previously identified neuronal molecules such as the WD40 domain protein QUI-1 and MACO-1 Macoilin, report new roles for nociceptive neurons in modulating pheromone-induced dauer formation, and identify tau tubulin kinases as new genes involved in dauer formation. Thus, phd mutants define loci required for the detection, transmission, or integration of pheromone signals in the regulation of dauer formation. © 2016 Neal et al.1

    Left-right olfactory asymmetry results from antagonistic functions of voltage-activated calcium channels and the Raw repeat protein OLRN-1 in C. elegans

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    <p>Abstract</p> <p>Background</p> <p>The left and right AWC olfactory neurons in <it>Caenorhabditis elegans </it>differ in their functions and in their expression of chemosensory receptor genes; in each animal, one AWC randomly takes on one identity, designated AWC<sup>OFF</sup>, and the contralateral AWC becomes AWC<sup>ON</sup>. Signaling between AWC neurons induces left-right asymmetry through a gap junction network and a claudin-related protein, which inhibit a calcium-regulated MAP kinase pathway in the neuron that becomes AWC<sup>ON</sup>.</p> <p>Results</p> <p>We show here that the asymmetry gene <it>olrn-1 </it>acts downstream of the gap junction and claudin genes to inhibit the calcium-MAP kinase pathway in AWC<sup>ON</sup>. OLRN-1, a protein with potential membrane-association domains, is related to the <it>Drosophila </it>Raw protein, a negative regulator of JNK mitogen-activated protein (MAP) kinase signaling. <it>olrn-1 </it>opposes the action of two voltage-activated calcium channel homologs, <it>unc-2 </it>(CaV2) and <it>egl-19 </it>(CaV1), which act together to stimulate the calcium/calmodulin-dependent kinase CaMKII and the MAP kinase pathway. Calcium channel activity is essential in AWC<sup>OFF</sup>, and the two AWC neurons coordinate left-right asymmetry using signals from the calcium channels and signals from <it>olrn-1</it>.</p> <p>Conclusion</p> <p><it>olrn-1 </it>and voltage-activated calcium channels are mediators and targets of AWC signaling that act at the transition between a multicellular signaling network and cell-autonomous execution of the decision. We suggest that the asymmetry decision in AWC results from the intercellular coupling of voltage-regulated channels, whose cross-regulation generates distinct calcium signals in the left and right AWC neurons. The interpretation of these signals by the kinase cascade initiates the sustained difference between the two cells.</p
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