The Caenorhabditis elegans innexin INX-20 regulates nociceptive behavioral sensitivity.

Autor:	Chaubey AH; Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA., Sojka SE; Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA., Onukwufor JO; Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA., Ezak MJ; Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA., Vandermeulen MD; Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA., Bowitch A; Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA., Vodičková A; Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA., Wojtovich AP; Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA.; Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA., Ferkey DM; Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.
Jazyk:	angličtina
Zdroj:	Genetics [Genetics] 2023 Apr 06; Vol. 223 (4).
DOI:	10.1093/genetics/iyad017
Abstrakt:	Organisms rely on chemical cues in their environment to indicate the presence or absence of food, reproductive partners, predators, or other harmful stimuli. In the nematode Caenorhabditis elegans, the bilaterally symmetric pair of ASH sensory neurons serves as the primary nociceptors. ASH activation by aversive stimuli leads to backward locomotion and stimulus avoidance. We previously reported a role for guanylyl cyclases in dampening nociceptive sensitivity that requires an innexin-based gap junction network to pass cGMP between neurons. Here, we report that animals lacking function of the gap junction component INX-20 are hypersensitive in their behavioral response to both soluble and volatile chemical stimuli that signal through G protein-coupled receptor pathways in ASH. We find that expressing inx-20 in the ADL and AFD sensory neurons is sufficient to dampen ASH sensitivity, which is supported by new expression analysis of endogenous INX-20 tagged with mCherry via the CRISPR-Cas9 system. Although ADL does not form gap junctions directly with ASH, it does so via gap junctions with the interneuron RMG and the sensory neuron ASK. Ablating either ADL or RMG and ASK also resulted in nociceptive hypersensitivity, suggesting an important role for RMG/ASK downstream of ADL in the ASH modulatory circuit. This work adds to our growing understanding of the repertoire of ways by which ASH activity is regulated via its connectivity to other neurons and identifies a previously unknown role for ADL and RMG in the modulation of aversive behavior. Competing Interests: Conflicts of interest None declared. (© The Author(s) 2023. Published by Oxford University Press on behalf of the Genetics Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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