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Transient Receptor Potential Channels and Itch
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Mahar Fatima, Jingyi Liu, Bo Duan
TRPM8 is a non-selective channel and somatic transducer for sensing temperature less than 28°C. Chemical compounds that elicit cooling sensation, such as menthol, icilin, and eucalyptol, can also activate TRPM8 channels (93–95). TRPM8 is expressed in lung epithelial cells, colon tissue, nasal mucosa, prostrate, scrotal skin, seminiferous tubules, testicles, cornea, Merkel cells, keratinocytes, and primary sensory neurons in the DRG and the TG, consistent with its predominant role in the detection of cool in mice (96,97).
Basic Thermal Physiology: What Processes Lead to the Temperature Distribution on the Skin Surface
Published in Kurt Ammer, Francis Ring, The Thermal Human Body, 2019
TRPA1 was localized in the peripheral nervous system and in the hair cells of the inner ear. A temperature less than 17°C activates the transient receptor potential thermally, cinnamaldehyde, main compound of cinnamon essential oil, mustard oil, allicin and icilin lead also to the activation of TRPA1.
Pharmacological approaches to treat intestinal pain
Published in Expert Review of Clinical Pharmacology, 2023
Mikolaj Swierczynski, Adam Makaro, Agata Grochowska, Maciej Salaga
Another receptor which mediates intestinal nociception is TRPM8 involved in the development of high-pressure induced pain. Mouse studies showed that inhibition of TRPM8 acts antinociceptive, which was indicated by decreased CGRP release. Mechanically-induced colonic pain responses were significantly decreased in TRPM8 knockout mice as well as in animals treated with TRPM8 antagonist administered i.p [110]. Moreover, the i.c. administration of TRPM8 agonist resulted in behavioral pain responses, which were markedly enhanced in mice with colitis. This pronociceptive effect was reduced by previous s.c. injection of TRPM8 antagonist [111]. Contrarily, some other studies showed that activation of TRPM8 by icilin produces anti-inflammatory effect. Additionally, TRPM8 expression is increased in colonic tissue obtained from IBD patients [112].
Emerging drugs for the treatment of bladder storage dysfunction
Published in Expert Opinion on Emerging Drugs, 2022
TRPM8 is a polymodal, Ca2+-permeant, and nonselective cation channel, identified as the physiological sensor of environmental cold. It is activated by cool temperatures (8–25°C) and by chemicals that provoke ‘cool’ sensations, such as menthol and icilin. TRPM8 is widely distributed in the body and predominantly expressed in a subpopulation of sensitive primary afferent neurons [71,72]. In the human bladder, Mukerji et al. [73] demonstrated TRPM8 expression in a subset of small nerve fibers. The channel was also expressed in dorsal root ganglion neurons innervating the rat bladder [74].
The triple function of the capsaicin-sensitive sensory neurons: In memoriam János Szolcsányi
Published in Temperature, 2023
Erika Pintér, Zsuzsanna Helyes, Éva Szőke, Kata Bölcskei, Angéla Kecskés, Gábor Pethő
Previous studies on TRP ion channels characterized important properties of these receptors but our knowledge about the potential function of the lipid rafts surrounding them in the plasma membrane is limited. After the description of lipid rafts, it has been reported that they have important functional significance for example around the nicotinic acetylcholine receptors or human 5-HT7 receptors [83–87] as microdomains rich in cholesterol, sphingomyelin and gangliosides. In the early 2000s few studies were published with controversial results about the role of lipid rafts in the function of TRPV1 channels. Cholesterol depletion by methyl β-cyclodextrin (MCD) did not result in any change in heat-induced currents of TRPV1-transfected Xenopus laevis oocytes [88], while in DRG neurons the magnitude of capsaicin-evoked currents was significantly reduced [89]. In contrast, it has been reported previously that cholesterol depletion did not modulate 3HRTX binding to TRPV1 receptors in rat C6 glioma cells [90]. Beyond cholesterol depletion other treatments are also suitable for disintegration of lipid rafts. Sphingomyelinase (SMase) depletes membrane sphingomyelin by hydrolysis of sphingomyelin to phosphocholine and ceramide [91,92]. The third mechanism for lipid raft disruption is to inhibit the glycosphingolipid synthesis by myriocin treatment [93,94]. The aim of our research group was to investigate whether the change in lipid rafts surrounding the TRP channels alters their chemical activation. We examined the rise in intracellular Ca2+ concentration in sensory neuronal culture, receptor-expressing cell line and performed fluorescence spectroscopy and filipin staining to examine the properties of plasma membrane of CHO cells after lipid raft disruptor treatments (Figure 3) [95]. We used different vanilloid and nonvanilloid activators of the TRPV1 channel and agonists of transient receptor potential ankyrin 1 (TRPA1) (allyl isothiocyanate, formaldehyde) under cholesterol, sphingomyelin or gangliosides depletion [95,96]. In transient receptor potential melastatin 8 (TRPM8) receptor activation the involvement of lipid rafts was proven, MCD treatment shifted the threshold for TRPM8 activation to a higher temperature [97]. TRPM8 and TRPM3 are also thermosensor TRP channels, menthol, icilin and temperatures below 26°C activate TRPM8 [98–101]. TRPM3 is expressed in a variety of neuronal and non-neuronal tissues, pregnenolone sulfate derived from cholesterol is a potent activator [102–105].