Cortical astrocytes rewire somatosensory cortical circuits for peripheral neuropathic pain

Kim, Sun Kwang; Hayashi, Hideaki; Ishikawa, Tatsuya; Shibata, Keisuke; Shigetomi, Eiji; Shinozaki, Youichi; Inada, Hiroyuki; Roh, Seung-Eon; Kim, Sang Jeong; Lee, Gihyun; Bae, Hyunsu; Moorhouse, Andrew J.; Mikoshiba, Katsuhiko; Fukazawa, Yugo; Koizumi, Schuichi; Nabekura, Junichi

doi:10.1172/jci82859

Cited by 156 publications

(202 citation statements)

References 68 publications

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“…3). Nerve injury also induces spinal cord and cortical astrocytes to up-regulate thrombospondin-4 (TSP4), which promotes neuropathic pain through the formation of new synapses and rewiring of somatosensory cortical circuits(40, 41). Notably, a single human astrocyte may contact more than 1 million synapses, and such complexity points to a more important role of astrocytes in humans that bears further investigation.…”

Section: Pain Modulation By Non-neuronal Cellsmentioning

confidence: 99%

Pain regulation by non-neuronal cells and inflammation

Chamessian

Zhang

2016

Science

974

821

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Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells, play active roles in the pathogenesis and resolution of pain. We review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain. Recent studies also suggest bacterial infections regulate pain through direct actions on sensory neurons, and specific receptors are present in nociceptors to detect danger signals from infections. We also discuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.

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Section: Pain Modulation By Non-neuronal Cellsmentioning

confidence: 99%

Pain regulation by non-neuronal cells and inflammation

Chamessian

Zhang

2016

Science

974

821

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“…4,5 Activated astrocytes may induce local neuroinflammation by promoting the release of inflammatory cytokines and chemokines, which sensitize the neurons and contribute to the generation of neuropathic pain. 6 Our previous study demonstrated the involvement of activated astrocytes in the generation of hyperalgesia.…”

mentioning

confidence: 99%

Kindlin-1 Regulates Astrocyte Activation and Pain Sensitivity in Rats With Neuropathic Pain

Zhao

Pan

2018

Regional Anesthesia and Pain Medicine

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“…This elicited Ca 2+ transients and the release of astrocytic TSP-1, which in turn activated neuronal α2δ1 receptors to induce new synapse formation. Blocking astrocytic Ca 2+ elevation or synaptic formation (using α2δ1 blocker gabapentin) suppressed neuropathy-triggered hypersensitivity 35 . These findings are interesting since gabapentin is used clinically.…”

Section: Astrocytesmentioning

confidence: 99%

“…Recent research resulted in interesting novel findings that considerably advance our understanding of neuropathic pain pathogenesis and offer numerous new intervention targets, including cytokines (CSF1) 15, 16 ; TMEM16F-mediated microglial phagocytosis 17 ; microglial enhancers 22 ; astrocytic connexin 43, CXCL13/CXCR5, or cortical synaptic plasticity 33– 35 ; oligodendrocyte-based signaling 40 ; G9a-mediated histone methylation 72, 73 ; and many ncRNAs 79– 85 . The key questions are which of these effects will be replicated and tested in patients and will any of them prove clinically effective.…”

Section: Open Questions Opportunities and Challengesmentioning

confidence: 99%

Recent advances in understanding neuropathic pain: glia, sex differences, and epigenetics

Machelska

Celik

2016

F1000Res

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Neuropathic pain results from diseases or trauma affecting the nervous system. This pain can be devastating and is poorly controlled. The pathophysiology is complex, and it is essential to understand the underlying mechanisms in order to identify the relevant targets for therapeutic intervention. In this article, we focus on the recent research investigating neuro-immune communication and epigenetic processes, which gain particular attention in the context of neuropathic pain. Specifically, we analyze the role of glial cells, including microglia, astrocytes, and oligodendrocytes, in the modulation of the central nervous system inflammation triggered by neuropathy. Considering epigenetics, we address DNA methylation, histone modifications, and the non-coding RNAs in the regulation of ion channels, G-protein-coupled receptors, and transmitters following neuronal damage. The goal was not only to highlight the emerging concepts but also to discuss controversies, methodological complications, and intriguing opinions.

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Cortical astrocytes rewire somatosensory cortical circuits for peripheral neuropathic pain

Cited by 156 publications

References 68 publications

Pain regulation by non-neuronal cells and inflammation

Pain regulation by non-neuronal cells and inflammation

Kindlin-1 Regulates Astrocyte Activation and Pain Sensitivity in Rats With Neuropathic Pain

Recent advances in understanding neuropathic pain: glia, sex differences, and epigenetics

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