Microglia–neuronal signalling in neuropathic pain hypersensitivity 2.0
Open accessAbstract
Microglia are increasingly recognized as critical in the pathogenesis of pain hypersensitivity caused by injury to peripheral nerves. The core signalling pathway is through P2X4 purinergic receptors on the microglia which, via the release of brain-derived neurotrophic factor, cause disinhibition of nociceptive dorsal horn neurons by raising intracellular chloride levels. This disinhibition works in synergy with enhanced excitatory synaptic transmission in the dorsal horn to transform the output of the nociceptive network. There is increased discharge output, unmasking of responses to innocuous peripheral inputs and spontaneous activity in neurons that otherwise only signal nociception. Together the changes caused by microglia-neuron signalling may account for the main symptoms of neuropathic pain in humans.
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Abnormal microglia function and complement cascade activation have been associated with neurodegeneration of the CNS.
“Consistent with this idea, abnormal microglia function and complement cascade activation have been associated with neurodegeneration of the CNS (Alexander et al., 2008; Beggs and Salter, 2010; Rosen and Stevens, 2010; Schafer and Stevens, 2010; Stephan et al. 2012).”
From Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012) · cites this paper as Beggs and Salter, 2010
The discussion of microglial signalling (p. 2) concerns pain hypersensitivity after peripheral nerve injury, while the Conclusions (p. 6) mention protective and pathological microglial roles in responses to CNS injury. Neither passage addresses complement cascade activation or an association with CNS neurodegeneration; searches for those terms found no supporting passage in our copy. (LLM, conf=0.76)
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- Authors
- Beggs, S., & Salter, M. W.
- Affiliations
- Hospital for Sick Children (CA)
- Corresponding author
- Salter, Michael W
- Venue
- Current Opinion in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2010-08
- Volume
- 20
- Issue
- 4
- Pages
- 474-480
- ISSN
- 0959-4388 (ISSN-L)
- PMC
- PMC3589562
- OpenAlex
- W2012369847
- Cited by
- 91
- References
- 36
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 2 · 2020: 7 · 2019: 6 · 2018: 4 · 2017: 10 · 2016: 10 · 2015: 2 · 2014: 6 · 2013: 7 · 2012: 13
- FWCI
- 1.01
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Current Opinion in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Canadian Institutes of Health Research (MT-12682)
- Topics
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- microglia, neuropathic pain, hyperalgesia, P2X4 receptor, purinergic signaling, brain-derived neurotrophic factor, dorsal horn neurons, chloride homeostasis, synaptic transmission, spontaneous neuronal activity, nociception, peripheral nerve injury
- MeSH terms
- Animals, Cell Communication, Chlorides, Humans, Models, Biological, Synaptic Transmission, Neuralgia, Neurons, Signal Transduction, Pain Threshold, Microglia, Brain-Derived Neurotrophic Factor, Receptors, Purinergic P2X4
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