Transient receptor potential ion channels in primary sensory neurons as targets for novel analgesics

• Published in: British journal of pharmacology 2014-05, Vol.171 (10), p.2508-2527
• Main Authors: Sousa‐Valente, J, Andreou, A P, Urban, L, Nagy, I
• Format: Article
• Language: English
• Subjects: Analgesics; Analgesics - pharmacology; Animals; Binding sites; Drug Design; Humans; inflammation; Membrane Transport Modulators - pharmacology; Molecular Targeted Therapy; nerve injury; Neurons; Nociception - drug effects; Nociceptive Pain - metabolism; Nociceptive Pain - physiopathology; Nociceptive Pain - prevention & control; Nociceptive Pain - psychology; Pain; Pain Threshold - drug effects; Sensory Receptor Cells - drug effects; Sensory Receptor Cells - metabolism; Signal Transduction - drug effects; Themed Section: The Pharmacology of Trp Channels; Transient Receptor Potential Channels - drug effects; Transient Receptor Potential Channels - metabolism; TRPA1; TRPM2; TRPM3; TRPM8; TRPV1; TRPV4
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/bph.12532

The last decade has witnessed an explosion in novel findings relating to the molecules involved in mediating the sensation of pain in humans. Transient receptor potential (TRP) ion channels emerged as the greatest group of molecules involved in the transduction of various physical stimuli into neuronal signals in primary sensory neurons, as well as, in the development of pain. Here, we review the role of TRP ion channels in primary sensory neurons in the development of pain associated with peripheral pathologies and possible strategies to translate preclinical data into the development of effective new analgesics. Based on available evidence, we argue that nociception‐related TRP channels on primary sensory neurons provide highly valuable targets for the development of novel analgesics and that, in order to reduce possible undesirable side effects, novel analgesics should prevent the translocation from the cytoplasm to the cell membrane and the sensitization of the channels rather than blocking the channel pore or binding sites for exogenous or endogenous activators. Linked Articles This article is part of a themed section on the pharmacology of TRP channels. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue‐10