The DOI matches its Crossref record; 168 of the 169 references it cites were found in a registry or an index.
Cellular and Molecular Mechanisms of Pain
Open accessAbstract
The nervous system detects and interprets a wide range of thermal and mechanical stimuli, as well as environmental and endogenous chemical irritants. When intense, these stimuli generate acute pain, and in the setting of persistent injury, both peripheral and central nervous system components of the pain transmission pathway exhibit tremendous plasticity, enhancing pain signals and producing hypersensitivity. When plasticity facilitates protective reflexes, it can be beneficial, but when the changes persist, a chronic pain condition may result. Genetic, electrophysiological, and pharmacological studies are elucidating the molecular mechanisms that underlie detection, coding, and modulation of noxious stimuli that generate pain.
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“In the presence of persistent damage, both the central and the peripheral components of pain pathway exhibit an extreme plasticity to produce hypersensitivity.”
From Pain and Evil: From Local Nociception to Misery Following Social Harm (2020) · cites this paper as [3]
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RetractedPain mechanisms: a new theory.
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The capsaicin receptor: a heat-activated ion channel in the pain pathway
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Self-citationCentral sensitization: a generator of pain hypersensitivity by central neural plasticity
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Self-citationHuman brain mechanisms of pain perception and regulation in health and disease
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Identification of a cold receptor reveals a general role for TRP channels in thermosensation
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Self-citationMolecular mechanisms of nociception
Julius, D., & Basbaum, A. I. (2001) · Nature · doi:10.1038/35093019 · Cited by 2,685 · cited 1×
“Nociceptors can also be distinguished according to their differential expression of channels that confer sensitivity to heat (TRPV1), cold (TRPM8), acidic milieu (ASICs), and a host of chemical irritants (TRPA1) (Julius and Basbaum, 2001).”
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Metadata
- Authors
- Basbaum, A. I., Bautista, D. M., Scherrer, G., & Julius, D.
- Affiliations
- University of California, San Francisco (US)
- University of California, Berkeley (US)
- Corresponding author
- Basbaum, Allan I.
- Julius, David
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 139
- Issue
- 2
- Pages
- 267-284
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2852643
- OpenAlex
- W2075715972
- Cited by
- 4,344
- References
- 169
- Citations by year
- 2026: 246 · 2025: 291 · 2024: 284 · 2023: 275 · 2022: 315 · 2021: 380 · 2020: 318 · 2019: 296 · 2018: 260 · 2017: 259 · 2016: 241 · 2015: 236 · 2014: 256 · 2013: 220 · 2012: 188
- FWCI
- 16.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1385 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS055299, R37NS047723)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- pain mechanisms, nociception, pain transmission, central sensitization, peripheral sensitization, chronic pain, pain plasticity, pain modulation
- MeSH terms
- Animals, Chronic Disease, Humans, Neuronal Plasticity, Nociceptors, Pain
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