- Section 1 Historical
- Section 2 Firsts
- Chapter 21 The key role of nerve growth factor in inflammatory pain processing
- Chapter 22 Mapping of neurotrophin receptors on adult sensory neurons
- Chapter 23 Plasticity in somatic receptive fields after nerve injury
- Chapter 24 Peripheral neural mechanisms of cutaneous heat hyperalgesia and heat pain
- Chapter 25 The cloning and characterization of the cannabinoid type 1 receptor
- Chapter 26 Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies
- Chapter 27 The capsaicin receptor
- Chapter 28 VR1 in inflammatory thermal hyperalgesia
- Chapter 29 A signature of pain in the brain
- Chapter 30 Cytokines as central to peripheral sensitization and hyperalgesia
- Chapter 31 Endogenous opioids mediate stress-induced analgesia
- Chapter 32 The first crystal structure of an ionotropic glutamate receptor ligand-binding core
- Chapter 33 Control of pain initiation by endogenous cannabinoids
- Chapter 34 Peripheral analgesia involves cannabinoid receptors
- Chapter 35 Glia
- Chapter 36 The challenges of animal models of pain
- Chapter 37 Mechanisms of bone cancer pain
- Chapter 38 The molecular structure of the <span xml:lang="ell">μ</span>-opioid receptor
- Chapter 39 The milestone effect of DNIC in our understanding of pain
- Chapter 40 The original description of central sensitization
- Chapter 41 The molecular basis for the placebo effect
- Section 3 Science
- Section 4 Clinical
- Section 5 Mechanisms
- Section 6 Neuropathic
- Section 7 Psychosocial
- Section 8 Genetics
(p. 100) The capsaicin receptor
- Chapter:
- (p. 100) The capsaicin receptor
- Author(s):
Istvan Nagy
- DOI:
- 10.1093/med/9780198834359.003.0027
The landmark paper discussed in this chapter is ‘The capsaicin receptor: A heat activated ion channel in the pain pathway’, published by Caterina et al. in 1997. The identification of the molecular basis for the sensitivity of a major proportion of nociceptive primary sensory neurons for capsaicin, the pungent agent in chilli pepper, was undoubtedly one of the most significant pain-related discoveries in the twentieth century, for at least three reasons. First, the mechanism for capsaicin-induced responses could unequivocally be explained. Second, the discovery heralded the starting point for the development of a highly promising, mechanism-based means of analgesia. Third, the discovery also sparked studies which resulted in the discovery of the major cation channel family, the transient receptor potential (TRP) ion channel family, several members of which have also become putative targets for the development of analgesics.
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- Section 1 Historical
- Section 2 Firsts
- Chapter 21 The key role of nerve growth factor in inflammatory pain processing
- Chapter 22 Mapping of neurotrophin receptors on adult sensory neurons
- Chapter 23 Plasticity in somatic receptive fields after nerve injury
- Chapter 24 Peripheral neural mechanisms of cutaneous heat hyperalgesia and heat pain
- Chapter 25 The cloning and characterization of the cannabinoid type 1 receptor
- Chapter 26 Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies
- Chapter 27 The capsaicin receptor
- Chapter 28 VR1 in inflammatory thermal hyperalgesia
- Chapter 29 A signature of pain in the brain
- Chapter 30 Cytokines as central to peripheral sensitization and hyperalgesia
- Chapter 31 Endogenous opioids mediate stress-induced analgesia
- Chapter 32 The first crystal structure of an ionotropic glutamate receptor ligand-binding core
- Chapter 33 Control of pain initiation by endogenous cannabinoids
- Chapter 34 Peripheral analgesia involves cannabinoid receptors
- Chapter 35 Glia
- Chapter 36 The challenges of animal models of pain
- Chapter 37 Mechanisms of bone cancer pain
- Chapter 38 The molecular structure of the <span xml:lang="ell">μ</span>-opioid receptor
- Chapter 39 The milestone effect of DNIC in our understanding of pain
- Chapter 40 The original description of central sensitization
- Chapter 41 The molecular basis for the placebo effect
- Section 3 Science
- Section 4 Clinical
- Section 5 Mechanisms
- Section 6 Neuropathic
- Section 7 Psychosocial
- Section 8 Genetics