scholarly journals Transient receptor potential ankyrin-1 has a major role in mediating visceral pain in mice

2010 ◽  
Vol 298 (1) ◽  
pp. G81-G91 ◽  
Author(s):  
Fiore Cattaruzza ◽  
Ian Spreadbury ◽  
Marcela Miranda-Morales ◽  
Eileen F. Grady ◽  
Stephen Vanner ◽  
...  
Keyword(s):  
Inflammatory Pain ◽  
Transient Receptor Potential ◽  
Visceral Pain ◽  
Receptor Potential ◽  
Afferent Neurons ◽  
Visceral Hyperalgesia ◽  
Spinal Neurons ◽  
Primary Afferent Neurons ◽  
Primary Afferent ◽  
Transient Receptor

The excitatory ion channel transient receptor potential ankyrin-1 (TRPA1) is prominently expressed by primary afferent neurons and is a mediator of inflammatory pain. Inflammatory agents can directly activate [e.g., hydroxynonenal (HNE), prostaglandin metabolites] or indirectly sensitize [e.g., agonists of protease-activated receptor (PAR2)] TRPA1 to induce somatic pain and hyperalgesia. However, the contribution of TRPA1 to visceral pain is unknown. We investigated the role of TRPA1 in visceral hyperalgesia by measuring abdominal visceromotor responses (VMR) to colorectal distention (CRD) after intracolonic administration of TRPA1 agonists [mustard oil (MO), HNE], sensitizing agents [PAR2 activating peptide (PAR2-AP)], and the inflammatory agent trinitrobenzene sulfonic acid (TNBS) in trpa1+/+ and trpa1−/− mice. Sensory neurons innervating the colon, identified by retrograde tracing, coexpressed immunoreactive TRPA1, calcitonin gene-related peptide, and substance P, expressed TRPA1 mRNA and responded to MO with depolarizing currents. Intracolonic MO and HNE increased VMR to CRD and induced immunoreactive c-fos in spinal neurons in trpa1 +/+ but not in trpa1 −/− mice. Intracolonic PAR2-AP induced mechanical hyperalgesia in trpa1 +/+ but not in trpa1 −/− mice. TNBS-induced colitis increased in VMR to CRD and induced c-fos in spinal neurons in trpa1 +/+ but not in trpa1 −/− mice. Thus TRPA1 is expressed by colonic primary afferent neurons. Direct activation of TRPA1 causes visceral hyperalgesia, and TRPA1 mediates PAR2-induced hyperalgesia. TRPA1 deletion markedly reduces colitis-induced mechanical hyperalgesia in the colon. Our results suggest that TRPA1 has a major role in visceral nociception and may be a therapeutic target for colonic inflammatory pain.

scholarly journals Highway to thermosensation: a traced review, from the proteins to the brain

2017 ◽  
Vol 28 (1) ◽  
pp. 45-57 ◽  
Author(s):  
Ivan Ezquerra-Romano ◽  
Angel Ezquerra
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Afferent Neurons ◽  
Primary Afferent Neurons ◽  
Temperature Changes ◽  
The World ◽  
Temperature Ranges ◽  
Transient Receptor ◽  
The Brain

AbstractTemperature maintenance and detection are essential for the survival and perpetuation of any species. This review is focused on thermosensation; thus a detailed and traced explanation of the anatomical and physiological characteristics of each component of this sensation is given. First, the proteins that react to temperature changes are identified; next, the nature of the neurons involved in thermosensation is described; and then, the pathways from the skin through the spinal cord to the brain are outlined. Finally, the areas of the brain and their interconnections where thermoperception arises are explained. Transduction of the external and internal temperature information is essentially mediated by the transient receptor potential ion channels (TRPs). These proteins are embedded in the neurons’ membrane and they hyper- or de-polarize neurons in function of the intrinsic voltage and the temperature changes. There are distinct TRP sensors for different temperature ranges. Interestingly, the primary afferent neurons have either cold or hot receptors, so they are dedicated separately to cold or hot sensation. The information is transmitted by different pathways from the skin to the brain, where it either remains separated or is integrated to generate a response. It seems that both the determination of how thermoperception is produced and how we interact with the world are dependent on the particular arrangement and nature of the components, the way of transduction of information and the communication between these elements.

scholarly journals Capsazepine decreases corneal pain syndrome in severe dry eye disease

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Darine Fakih ◽  
Adrian Guerrero-Moreno ◽  
Christophe Baudouin ◽  
Annabelle Réaux-Le Goazigo ◽  
Stéphane Mélik Parsadaniantz
Keyword(s):  
In Situ Hybridization ◽  
Inflammatory Pain ◽  
Transient Receptor Potential ◽  
Ex Vivo ◽  
Receptor Potential ◽  
Eye Disease ◽  
Ocular Pain ◽  
Trpv1 Antagonist ◽  
Transient Receptor

Abstract Background Dry eye disease (DED) is a multifactorial disease of the ocular surface accompanied by neurosensory abnormalities. Here, we evaluated the effectiveness of transient receptor potential vanilloid-1 (TRPV1) blockade to alleviate ocular pain, neuroinflammation, and anxiety-like behavior associated with severe DED. Methods Chronic DED was induced by unilateral excision of the Harderian and extraorbital lacrimal glands of adult male mice. Investigations were conducted at 21 days after surgery. The mRNA levels of TRPV1, transient receptor potential ankyrin-1 (TRPA1), and acid-sensing ion channels 1 and 3 (ASIC1 and ASIC3) in the trigeminal ganglion (TG) were evaluated by RNAscope in situ hybridization. Multi-unit extracellular recording of ciliary nerve fiber activity was used to monitor spontaneous and stimulated (cold, heat, and acid) corneal nerve responsiveness in ex vivo eye preparations. DED mice received topical instillations of the TRPV1 antagonist (capsazepine) twice a day for 2 weeks from d7 to d21 after surgery. The expression of genes involved in neuropathic and inflammatory pain was evaluated in the TG using a global genomic approach. Chemical and mechanical corneal nociception and spontaneous ocular pain were monitored. Finally, anxiety-like behaviors were assessed by elevated plus maze and black and white box tests. Results First, in situ hybridization showed DED to trigger upregulation of TRPV1, TRPA1, ASIC1, and ASIC3 mRNA in the ophthalmic branch of the TG. DED also induced overexpression of genes involved in neuropathic and inflammatory pain in the TG. Repeated instillations of capsazepine reduced corneal polymodal responsiveness to heat, cold, and acidic stimulation in ex vivo eye preparations. Consistent with these findings, chronic capsazepine instillation inhibited the upregulation of genes involved in neuropathic and inflammatory pain in the TG of DED animals and reduced the sensation of ocular pain, as well as anxiety-like behaviors associated with severe DED. Conclusion These data provide novel insights on the effectiveness of TRPV1 antagonist instillation in alleviating abnormal corneal neurosensory symptoms induced by severe DED, opening an avenue for the repositioning of this molecule as a potential analgesic treatment for patients suffering from chronic DED.

Transient receptor potential ankyrin-1 participates in visceral hyperalgesia following experimental colitis

2008 ◽  
Vol 440 (3) ◽  
pp. 237-241 ◽  
Author(s):  
Jing Yang ◽  
Yanqing Li ◽  
Xiuli Zuo ◽  
Yanbo Zhen ◽  
Yanbo Yu ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Experimental Colitis ◽  
Visceral Hyperalgesia ◽  
Transient Receptor

39. Transient Receptor Potential A1 (TRPA1) Mediates Pancreatic Inflammatory Pain

2008 ◽  
Vol 144 (2) ◽  
pp. 192-193
Author(s):  
Eugene P. Ceppa ◽  
Natalya Vaksman ◽  
Eileen F. Grady ◽  
Nigel W. Bunnett ◽  
Kimberly S. Kirkwood
Keyword(s):  
Inflammatory Pain ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential A1 ◽  
Transient Receptor
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