Nociception

Honjo, Ken; Robertson, Jessica; Tracey, W. Daniel

doi:10.1017/cbo9780511920585.006

Cited by 2 publications

(2 citation statements)

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“…Thermal nociception assays were as described previously ( Honjo et al, 2014 , 2016 ). In a primary screen, approximately 10–20 lines were tested per day and each day included a control cross for the driver line to the relevant isogenic background ( md-Gal4/+;UAS-Dicer 2/+ ).…”

Section: Star*methodsmentioning

confidence: 99%

The Drosophila Small Conductance Calcium-Activated Potassium Channel Negatively Regulates Nociception

Mauthner

Tsubouchi

et al. 2018

Cell Reports

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Inhibition of nociceptor activity is important for the prevention of spontaneous pain and hyperalgesia. To identify the critical K channels that regulate nociceptor excitability, we performed a forward genetic screen using a Drosophila larval nociception paradigm. Knockdown of three K channel loci, the small conductance calcium-activated potassium channel (SK), seizure, and tiwaz, causes marked hypersensitive nociception behaviors. In more detailed studies of SK, we found that hypersensitive phenotypes can be recapitulated with a genetically null allele. Optical recordings from nociceptive neurons showed a significant increase in mechanically activated Ca signals in SK mutant nociceptors. SK is expressed in peripheral neurons, including nociceptive neurons. Interestingly, SK proteins localize to axons of these neurons but are not detected in dendrites. Our findings suggest a major role for SK channels in the regulation of nociceptor excitation and are inconsistent with the hypothesis that the important site of action is within dendrites.

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Section: Star*methodsmentioning

confidence: 99%

The Drosophila Small Conductance Calcium-Activated Potassium Channel Negatively Regulates Nociception

Mauthner

Tsubouchi

et al. 2018

Cell Reports

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“…Genetics screens for mutants and genes required for this behavior makes Drosophila larvae a robust system for identifying the molecular mechanisms of nociception. Moreover, many fly nociception genes are conserved in mammals (Woolf et al, 1997; Kang et al, 2010; Neely et al, 2010; Honjo et al, 2014; Jo et al, 2017),…”

Section: Introductionmentioning

confidence: 99%

The Drosophila gene smoke alarm regulates nociceptor-epidermis interactions and thermal nociception behavior

Mauthner

Fisher

2021

Preprint

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The detection and processing of noxious sensory input depends on the proper growth and function of nociceptor sensory neurons in the peripheral nervous system. In Drosophila melanogaster, the class IV (cIV) multidendritic dendritic arborization (md-da) neurons detect noxious stimuli through their highly branched dendrites that innervate the epidermis of the larval body wall. Here, we describe requirements of a previously uncharacterized gene named smoke alarm (smal), a discoidin domain receptor, in cIV md-da dendrite morphogenesis and nociception behavior. We find that smal mutant larvae exhibit thermal hyperalgesia that is fully rescued with a BAC transgene containing smal. Consistent with this phenotype, a smal reporter gene was expressed in nociceptors and other peripheral sensory neurons. Smal::GFP protein localized to punctate structures throughout the cIV md-da neurons. We further show that smal loss-of-function results in reduced nociceptor dendrite branching. Interestingly, mammalian homologues of smal act as collagen receptors, and we find that smal mutant dendrites showed an increase in epidermal cell ensheathment relative to animals that are wild type for smal. Based on this phenotype we propose that Smal protein function is required for attachment of dendrites to the extracellular matrix (ECM) and the loss of activity results in thermal hyperalgesia.

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Nociception

Cited by 2 publications

References 85 publications

The Drosophila Small Conductance Calcium-Activated Potassium Channel Negatively Regulates Nociception

The Drosophila Small Conductance Calcium-Activated Potassium Channel Negatively Regulates Nociception

The Drosophila gene smoke alarm regulates nociceptor-epidermis interactions and thermal nociception behavior

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