- 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. 120) Control of pain initiation by endogenous cannabinoids
- Chapter:
- (p. 120) Control of pain initiation by endogenous cannabinoids
- Author(s):
Andrea G. Hohmann
- DOI:
- 10.1093/med/9780198834359.003.0033
The landmark paper discussed in this chapter, published by Calignano et al. in 1998, focuses on the control of pain initiation by endogenous cannabinoids. In the paper, analgesic lipid mediators are shown to be present in peripheral paw tissue where they control the ability of pain signals to ascend to the central nervous system (CNS). Anandamide acts through a peripheral mechanism to suppress inflammatory pain via cannabinoid type 1 receptors. Palmitoylethanolamine, subsequently identified as an endogenous ligand for peroxisome proliferator-activated receptor-α, produces peripheral antinociceptive effects via a mechanism similar to that for the cannabinoid type 2 receptor. These lipids do not serve redundant functions and, in combination, produce synergistic antinociceptive effects. These observations suggested that drug-development efforts targeting peripheral control of pain may elucidate improved pharmacotherapies that lack the unwanted CNS side effects of current treatments.
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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