Differential Effects of TRPA and TRPV Channels on Behaviors of<i>Caenorhabditis elegans</i>

Thies, Jennifer L.; Neutzler, Vanessa; O'Leary, Fidelma A.; Li, He

doi:10.4137/jen.s32837

Cited by 4 publications

(3 citation statements)

References 23 publications

(26 reference statements)

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“…Thus, these data suggest some overlapping functions of DjTRPAa and DjTRPVab to mediate anandamide-sensing in D. japonica. Similar overlapping or interacting functions of TRPA1 and TRPV1 have previously been suggested in several other systems, including mouse (31), nematodes (58) and the medicinal leech (39).…”

Section: Resultssupporting

confidence: 73%

Pharmacological or genetic targeting of Transient Receptor Potential (TRP) channels can disrupt the planarian escape response

Sabry

Ireland

et al. 2019

Preprint

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25In response to noxious stimuli, planarians cease their typical ciliary gliding and exhibit 26 an oscillatory type of locomotion called scrunching. We have previously characterized the 27 biomechanics of scrunching and shown that it is induced by specific stimuli, such as 28 amputation, noxious heat, and extreme pH. Because these specific inducers are known to 29 activate Transient Receptor Potential (TRP) channels in other systems, we hypothesized that 30 TRP channels control scrunching. We found that chemicals known to activate TRPA1 (allyl 31 isothiocyanate (AITC) and hydrogen peroxide) and TRPV (capsaicin and anandamide) in other 32 systems induce scrunching in the planarian species Dugesia japonica and, except for 33 anandamide, in Schmidtea mediterranea. To confirm that these responses were specific to 34 either TRPA1 or TRPV, respectively, we tried to block scrunching using selective TRPA1 or 35 TRPV antagonists and RNA interference (RNAi) mediated knockdown. Unexpectedly, co-36 treatment with a mammalian TRPA1 antagonist, HC-030031, enhanced AITC-induced 37 scrunching by decreasing the latency time, suggesting an agonistic relationship in planarians. 38 We further confirmed that TRPA1 in both species is necessary for AITC-induced scrunching 39 using RNAi. Conversely, while co-treatment of a mammalian TRPV antagonist, SB-366791, 40 also enhanced capsaicin-induced reactions in D. japonica, combined knockdown of two 41 previously identified D. japonica TRPV genes (DjTRPVa and DjTRPVb) did not inhibit 42 capsaicin-induced scrunching. Surprisingly, RNAi of either DjTRPAa or DjTRPVa/DjTRPVb 43 disrupted scrunching induced by the endocannabinoid and TRPV agonist, anandamide. 44 Overall, our results show that although scrunching induction can involve different initial 45 pathways for sensing stimuli, this behavior's signature dynamical features are independent of 46 the inducer, implying that scrunching is a stereotypical planarian escape behavior in response 47 to various noxious stimuli that converge on a single downstream pathway. Understanding 48 which aspects of nociception are conserved or not across different organisms can provide 49 3 insight into the underlying regulatory mechanisms to better understand pain sensation. 50 51 52Normal locomotion of freshwater planarians, termed gliding, is achieved through 53 synchronous beating of cilia in a layer of secreted mucus (1-3). Gliding planarians display a 54 smooth motion without major body shape changes, except for turning movements of the 55 anterior end. However, when exposed to certain noxious stimuli (e.g. low pH, high temperature, 56 or amputation), planarians switch to a muscular-based escape gait that is characterized by 57 oscillatory body length changes (4). We termed this gait scrunching and showed that it has a 58 characteristic set of 4 quantifiable parameters: 1. frequency of body length oscillations, 2. 59 relative speed, 3. maximum amplitude, and 4. asymmetry of body elongation and contraction 60 (4). Moreover, scrunching is conserve...

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Section: Resultssupporting

confidence: 73%

Pharmacological or genetic targeting of Transient Receptor Potential (TRP) channels can disrupt the planarian escape response

Sabry

Ireland

et al. 2019

Preprint

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“…Consequently, C. elegans is a commonly used model organism to examine heat avoidance [5,[7][8][9]. Recently, we demonstrated C. elegans ability to avoid noxious heat is strongly associated with the FLP-18/FLP-21/NPR-1 neuropeptide signaling pathways but results also suggested that other neuropeptides signaling pathways or classical neurotransmitters are most likely playing an important role [7].…”

Section: Introductionmentioning

confidence: 96%

Impaired EAT-4 Vesicular Glutamate Transporter Leads to Defective Nocifensive Response of Caenorhabditis elegans to Noxious Heat

Leonelli

Nkambeu

Beaudry

2019

Preprint

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In mammals, glutamate is an important excitatory neurotransmitter. Glutamate and glutamate receptors are found in areas of the periphery, spinal cord and brain specifically involved in pain sensation, transmission and transduction. In C. elegans, several studies have suggested glutamate pathways are associated with withdrawal responses to mechanical stimuli and to chemical repellents. However, very few evidences demonstrate that glutamate pathways are important to mediate nocifensive response to noxious heat.The thermal avoidance behavior of C. elegans was studied and results illustrated that mutants of glutamate receptors (glr-1, glr-2, nmr-1, nmr-2) thermal avoidance was not affected. However, results revealed that all strains of eat-4 mutants, C. elegans vesicular glutamate transporters, displayed defective thermal avoidance behavior. Due to the interplay between the glutamate and the FLP-18/FLP-21/NPR-1 pathways, we analyzed the effectors FLP-18 and FLP-21 at the protein levels we have not observed biologically significant differences compared to N2 (WT) strain (fold-change < 2) except for the IK602 strain. The data presented in this manuscript reveals that glutamate signaling pathways are essential to elicit a nocifensive response to noxious heat in C. elegans.

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“…C. elegans is specifically suitable to study nociception as it exhibits a well-defined and reproducible nocifensive behavior, involving a reversal and change in direction away from the noxious stimulus [5][6][7]. Consequently, C. elegans is a commonly used model organism to examine heat avoidance [5,[7][8][9]. Following the genome sequencing of C. elegans, some genes were classified as Transient Receptor Potential (TRP) ion channel proteins with important sequence homologies to mammalian TRP channels including Transient Receptor Potential Vanilloid Channels (TRPVs) [5].…”

Section: Introductionmentioning

confidence: 99%

Impaired EAT-4 Vesicular Glutamate Transporter Leads to Defective Nocifensive Response of Caenorhabditis elegans to Noxious Heat

2020

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In mammals, glutamate is an important excitatory neurotransmitter. Glutamate and glutamate receptors are found in areas specifically involved in pain sensation, transmission and transduction such as peripheral nervous system, spinal cord and brain. In C. elegans, several studies have suggested glutamate pathways are associated with withdrawal responses to mechanical stimuli and to chemical repellents. However, few evidences demonstrate that glutamate pathways are important to mediate nocifensive response to noxious heat. The thermal avoidance behavior of C. elegans was studied and results illustrated that mutants of glutamate receptors (glr-1, glr-2, nmr-1, nmr-2) behaviors was not affected. However, results revealed that all strains of eat-4 mutants, C. elegans vesicular glutamate transporters, displayed defective thermal avoidance behaviors. Due to the interplay between the glutamate and the FLP-18/FLP-21/NPR-1 pathways, we analyzed the effectors FLP-18 and FLP-21 at the protein level, we did not observebiologically significant differences compared to N2 (WT) strain (fold-change < 2) except for the IK602 strain. The data presented in this manuscript reveals that glutamate signaling pathways are essential to elicit a nocifensive response to noxious heat in C. elegans.

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Differential Effects of TRPA and TRPV Channels on Behaviors ofCaenorhabditis elegans

Cited by 4 publications

References 23 publications

Pharmacological or genetic targeting of Transient Receptor Potential (TRP) channels can disrupt the planarian escape response

Pharmacological or genetic targeting of Transient Receptor Potential (TRP) channels can disrupt the planarian escape response

Impaired EAT-4 Vesicular Glutamate Transporter Leads to Defective Nocifensive Response of Caenorhabditis elegans to Noxious Heat

Impaired EAT-4 Vesicular Glutamate Transporter Leads to Defective Nocifensive Response of Caenorhabditis elegans to Noxious Heat

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