Nociceptor sensitization in pain pathogenesis

By M. Gold, G. Gebhart. Nature Medicine, 2010

845 citations recorded by the source corpus.

The incidence of chronic pain is estimated to be 20–25% worldwide. Few patients with chronic pain obtain complete relief from the drugs that are currently available, and more than half report inadequate relief. Underlying the challenge of developing better drugs to manage chronic pain is incomplete understanding of the heterogeneity of mechanisms that contribute to the transition from acute tissue insult to chronic pain and to pain conditions for which the underlying pathology is not apparent. An intact central nervous system (CNS) is required for the conscious perception of pain, and changes in the CNS are clearly evident in chronic pain states. However, the blockage of nociceptive input into the CNS can effectively relieve or markedly attenuate discomfort and pain, revealing the importance of ongoing peripheral input to the maintenance of chronic pain. Accordingly, we focus here on nociceptors: their excitability, their heterogeneity and their role in initiating and maintaining pain.

Subfields: Molecular Biology, Physiology, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/12aeb69f861291c3e2d1d23e1413aab4470f712b

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Citations in the corpus

Report Nociceptive Sensitization Reduces Predation Risk (2014, neutral): “Although neural mechanisms of nociceptive sensitization have received extensive study in the contexts of pain [18, 19] and aversive learning [20, 21], and its adaptive value for recuperative behavior, contextual learning, and defense against potential attackers has been conjectured [1, 22–24], until”
Multimodal contributions to body representation (2016, background): “In the afferent nociceptive and somatosensory pathways, deep synaptic and molecular membrane reorganization processes occur following either chronic neuropathic pain or deafferentation (Gold and Gebhart, 2010).”
TFOS DEWS II pain and sensation report (2017, neutral): “The events triggered by proinflammatory agents are diverse and complex [347,352].”
An artificial nociceptor based on a diffusive memristor (2018, background): “In contrast, the sensitivity of nociceptor increases if the stimulus is excessively intense and results in tissue damage (known as sensitization 9,10 ).”
Glia and pain: Is chronic pain a gliopathy? (2013, neutral): “Published by Elsevier B.V.”