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Molecular Basis of Infrared Detection by Snakes

ABSTRACT: Snakes possess a unique sensory system for detecting infrared radiation, enabling them to generate a ‘thermal image’ of predators or prey. Infrared signals are initially received by the pit organ, a highly specialized facial structure that is innervated by nerve fibers of the somatosensory system. How this organ detects and transduces infrared signals into nerve impulses is not known. Here we use an unbiased transcriptional profiling approach to identify TRPA1 as the infrared receptor on sensory neurons that innervate the pit organ. TRPA1 from pit bearing snakes (rattlesnakes and pythons) are the most heat sensitive vertebrate ion channels thus far identified, consistent with their role as primary transducers of infrared stimuli in these animals. Thus, snakes detect infrared signals through a mechanism involving radiant heating of the pit organ, rather than photochemical transduction. These findings illustrate the broad evolutionary tuning of TRP channels as thermosensors in the vertebrate nervous system.

ORGANISM(S): Python regius Masticophis flagellum testaceus Crotalus atrox Pantherophis obsoletus lindheimeri Corallus hortulana

PROVIDER: GSE19911 | GEO | 2010/03/16

SECONDARY ACCESSION(S): PRJNA121945

REPOSITORIES: GEO

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Molecular Basis of Infrared Detection by Snakes

Project description:Snakes possess a unique sensory system for detecting infrared radiation, enabling them to generate a ‘thermal image’ of predators or prey. Infrared signals are initially received by the pit organ, a highly specialized facial structure that is innervated by nerve fibers of the somatosensory system. How this organ detects and transduces infrared signals into nerve impulses is not known. Here we use an unbiased transcriptional profiling approach to identify TRPA1 as the infrared receptor on sensory neurons that innervate the pit organ. TRPA1 from pit bearing snakes (rattlesnakes and pythons) are the most heat sensitive vertebrate ion channels thus far identified, consistent with their role as primary transducers of infrared stimuli in these animals. Thus, snakes detect infrared signals through a mechanism involving radiant heating of the pit organ, rather than photochemical transduction. These findings illustrate the broad evolutionary tuning of TRP channels as thermosensors in the vertebrate nervous system. Gene expression measurements implicate TRPA1 as the heat-sensitive channel in diverse pit snakes

2010-03-16 | E-GEOD-19911 | biostudies-arrayexpress

Alternative splicing of the TRPV1 gene underlies infrared sensation in vampire bats

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Alternative splicing of the TRPV1 gene underlies infrared sensation in vampire bats

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Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation II

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Project description:Chronic pain can be debilitating, and current treatments are neither universally efficacious, nor without risks. New therapeutic options are needed. Transient receptor potential (TRP) ion channels regulate inflammation and pain. Understanding how endogenous TRP ligands regulate inflammation and pain may provide insights for new therapies. Spinal nerve ligation (SNL) injury was used as a model for chronic pain. Transcriptomic and targeted lipidomic analysis of damaged tissue revealed time-dependent increases in Cyp1b1 mRNA and a concurrent accumulation of 8,9-EET and 19,20-EpDPA post injury. Production of 8,9-EET and 19,20-EpDPA by human CYP1B1 and mouse Cyp1b1 was confirmed in vitro. 8,9-EET and 19,20-EpDPA selectively and dose-dependently sensitized and activated TRPA1 in overexpressing HEK-293 cells and Trpa1-expressing/AITC-responsive cultured mouse peptigergic DRG neurons. Activation of TRPA1 was attenuated by the antagonist A967079, and mouse Trpa1 was more responsive to agonists including 8,9-EET and 19,20-EpDPA than human TRPA1. This latter effect was mediated in part by amino acids Y933, G939, and S921. Intra-plantar injection of 19,20-EpDPA induced acute mechanical, but not thermal hypersensitivity in mice, which was blocked by A967079. Similarly, Cyp1b1 knockout mice displayed a reduced chronic pain phenotype, indicating a role for Cyp1b1-derived oxylipins in promoting Trpa1 activation and pain. Manipulation of the CYP1B1-oxylipin-TRPA1 axis following nerve injury could have therapeutic benefit.

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