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

• Published in: bioRxiv
• Main Authors: Leonelli, Sophie, Nkambeu, Bruno, Beaudry, Francis
• Format: Paper
• Language: English
• Published: Cold Spring Harbor Cold Spring Harbor Laboratory Press 11.01.2020
• Subjects: Avoidance behavior; Glutamic acid receptors; Glutamic acid transporter; Heat; Mechanical stimuli; Pain perception; Repellents; Signal transduction; Spinal cord; Worms
• DOI: 10.1101/620302

In mammal, 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, it has not been demonstrated that glutamate pathways are important to mediate nocifensive response to noxious heat. The data presented in this manuscript reveals for the first time that glutamate signaling pathways are essential to elicit a nocifensive response to noxious heat in C. elegans. Footnotes * 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.