- 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. 127) Glia: A new pain target
- Chapter:
- (p. 127) Glia: A new pain target
- Author(s):
Marzia Malcangio
- DOI:
- 10.1093/med/9780198834359.003.0035
The landmark review discussed in this chapter, published in 2003 by Watkins and Maier, showed how glia have a major role in the modulation of pain mechanisms in the spinal cord and act remotely from peripheral nerve injury. This review led the way to a substantial body of literature demonstrating the pivotal role played by both microglia and astrocytes in chronic pain mechanisms. Since 2003 the modalities underlying neuron–microglia communication (e.g. chemokines, proteases, the translocator protein TSPO) have been dissected, and novel pathways of interactions delineated. Concrete molecular targets expressed by spinal microglia in response to a remote injury have been identified and they hold promise for future analgesic therapies for chronic pain.
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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